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@article{Irizarry2005,
author = {Irizarry, Rafael A and Warren, Daniel and Spencer, Forrest and Kim, Irene F and Biswal, Shyam and Frank, Bryan C and Gabrielson, Edward and Garcia, Joe G N and Geoghegan, Joel and Germino, Gregory and Griffin, Constance and Hilmer, Sara C and Hoffman, Eric and Jedlicka, Anne E and Kawasaki, Ernest and Mart, Francisco and Morsberger, Laura and Lee, Hannah and Petersen, David and Quackenbush, John and Scott, Alan and Wilson, Michael},
doi = {10.1038/NMETH756},
file = {:Users/rikutakei/Downloads/papers/nmeth756.pdf:pdf},
journal = {Nat. Methods},
number = {5},
pages = {345--349},
title = {{Multiple-laboratory comparison of microarray platforms}},
volume = {2},
year = {2005}
}
@article{VanderHeiden2009,
author = {{Vander Heiden}, Matthew G and Cantley, Lewis C and Thompson, Craig B and Mammalian, Proliferating and Exhibit, Cells and Metabolism, Anabolic},
doi = {10.1126/science.1160809},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Vander Heiden et al. - 2009 - Understanding the Warburg Effect The metabolic requirements of cell proliferation.pdf:pdf},
journal = {Science (80-. ).},
keywords = {cancer,energy},
mendeley-tags = {cancer,energy},
number = {May},
pages = {1029--1034},
title = {{Understanding the Warburg Effect : The metabolic requirements of cell proliferation}},
volume = {324},
year = {2009}
}
@article{Gautier2004,
abstract = {MOTIVATION The processing of the Affymetrix GeneChip data has been a recent focus for data analysts. Alternatives to the original procedure have been proposed and some of these new methods are widely used. RESULTS The affy package is an R package of functions and classes for the analysis of oligonucleotide arrays manufactured by Affymetrix. The package is currently in its second release, affy provides the user with extreme flexibility when carrying out an analysis and make it possible to access and manipulate probe intensity data. In this paper, we present the main classes and functions in the package and demonstrate how they can be used to process probe-level data. We also demonstrate the importance of probe-level analysis when using the Affymetrix GeneChip platform.},
author = {Gautier, Laurent and Cope, Leslie and Bolstad, Benjamin M. and Irizarry, Rafael A.},
doi = {10.1093/bioinformatics/btg405},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Gautier et al. - 2004 - Affy - Analysis of Affymetrix GeneChip data at the probe level.pdf:pdf},
isbn = {1367-4803 (Print)$\backslash$r1367-4803 (Linking)},
issn = {13674803},
journal = {Bioinformatics},
number = {3},
pages = {307--315},
pmid = {14960456},
title = {{Affy - Analysis of Affymetrix GeneChip data at the probe level}},
volume = {20},
year = {2004}
}
@article{Lim2012,
abstract = {Background Quantification of the disease burden caused by different risks informs prevention by providing an account of health loss different to that provided by a disease-by-disease analysis. No complete revision of global disease burden caused by risk factors has been done since a comparative risk assessment in 2000, and no previous analysis has assessed changes in burden attributable to risk factors over time. Methods We estimated deaths and disability-adjusted life years; DALYs; sum of years lived with disability [YLD] and years of life lost [YLL]) attributable to the independent effects of 67 risk factors and clusters of risk factors for 21 regions in 1990 and 2010. We estimated exposure distributions for each year, region, sex, and age group, and relative risks per unit of exposure by systematically reviewing and synthesising published and unpublished data. We used these estimates, together with estimates of cause-specific deaths and DALYs from the Global Burden of Disease Study 2010, to calculate the burden attributable to each risk factor exposure compared with the theoretical-minimum-risk exposure. We incorporated uncertainty in disease burden, relative risks, and exposures into our estimates of attributable burden. Findings In 2010, the three leading risk factors for global disease burden were high blood pressure (7 0{\%} [95{\%} uncertainty interval 6 2-7 7] of global DALYs); tobacco smoking including second-hand smoke (6 3{\%} [5 5-7 0]), and alcohol use (5 5{\%} [5 0-5 9]). In 1990, the leading risks were childhood underweight (7 9{\%} [6 8-9 4]), household air pollution from solid fuels; (HAP; 7 0{\%} [5 6-8 3]), and tobacco smoking including second-hand smoke (6 1{\%} [5 4-6 8]). Dietary risk factors and physical inactivity collectively accounted for 10 0{\%} (95{\%} UI 9 2-10 8) of global DALYs in 2010, with the most prominent dietary risks being diets low in fruits and those high in sodium. Several risks that primarily affect childhood communicable diseases, including unimproved water and sanitation and childhood micronutrient deficiencies, fell in rank between 1990 and 2010, with unimproved water ' and sanitation accounting for 0 9{\%} (0 4-1 6) of global DALYs in 2010. However, in most of sub-Saharan Africa childhood underweight, HAP, and non-exclusive and discontinued breastfeeding were the leading risks in 2010, while HAP was the leading risk in south Asia. The leading risk factor in Eastern Europe, most of Latin America, and southern sub-Saharan Africa in 2010 was alcohol use; in most of Asia, North Africa and Middle East, and central Europe it was high blood pressure. Despite declines, tobacco smoking including second-hand smoke remained the leading risk in high-income north America and western Europe. High body-mass index has increased globally and it is the leading risk in Australasia and southern Latin America, and also ranks high in other high-income regions, North Africa and Middle East, and Oceania. Interpretation Worldwide, the contribution of different risk factors to disease burden has changed substantially, with a shift away from risks for communicable diseases in children towards those for non-communicable diseases in adults. These changes are related to the ageing population, decreased mortality among children younger than 5 years, changes in cause-of-death composition, and changes in risk factor exposures. New evidence has led to changes in the magnitude of key risks including unimproved water and sanitation, vitamin A and zinc deficiencies, and ambient particulate matter pollution. The extent to which the epidemiological shift has occurred and what the leading risks currently are varies greatly across regions. In much of sub-Saharan Africa, the leading risks are still those associated with poverty and those that affect children.},
author = {Lim, Stephen S. and Vos, Theo and Flaxman, Abraham D. and Danaei, Goodarz and Shibuya, Kenji and Adair-Rohani, Heather and Amann, Markus and Anderson, H. Ross and Andrews, Kathryn G. and Aryee, Martin and Atkinson, Charles and Bacchus, Loraine J. and Bahalim, Adil N. and Balakrishnan, Kalpana and Balmes, John and Barker-Collo, Suzanne and Baxter, Amanda and Bell, Michelle L. and Blore, Jed D. and Blyth, Fiona and Bonner, Carissa and Borges, Guilherme and Bourne, Rupert and Boussinesq, Michel and Brauer, Michael and Brooks, Peter and Bruce, Nigel G. and Brunekreef, Bert and Bryan-Hancock, Claire and Bucello, Chiara and Buchbinder, Rachelle and Bull, Fiona and Burnett, Richard T. and Byers, Tim E. and Calabria, Bianca and Carapetis, Jonathan and Carnahan, Emily and Chafe, Zoe and Charlson, Fiona and Chen, Honglei and Chen, Jian Shen and Cheng, Andrew Tai Ann and Child, Jennifer Christine and Cohen, Aaron and Colson, K. Ellicott and Cowie, Benjamin C. and Darby, Sarah and Darling, Susan and Davis, Adrian and Degenhardt, Louisa and Dentener, Frank and {Des Jarlais}, Don C. and Devries, Karen and Dherani, Mukesh and Ding, Eric L. and Dorsey, E. Ray and Driscoll, Tim and Edmond, Karen and Ali, Suad Eltahir and Engell, Rebecca E. and Erwin, Patricia J. and Fahimi, Saman and Falder, Gail and Farzadfar, Farshad and Ferrari, Alize and Finucane, Mariel M. and Flaxman, Seth and Fowkes, Francis Gerry R and Freedman, Greg and Freeman, Michael K. and Gakidou, Emmanuela and Ghosh, Santu and Giovannucci, Edward and Gmel, Gerhard and Graham, Kathryn and Grainger, Rebecca and Grant, Bridget and Gunnell, David and Gutierrez, Hialy R. and Hall, Wayne and Hoek, Hans W. and Hogan, Anthony and Hosgood, H. Dean and Hoy, Damian and Hu, Howard and Hubbell, Bryan J. and Hutchings, Sally J. and Ibeanusi, Sydney E. and Jacklyn, Gemma L. and Jasrasaria, Rashmi and Jonas, Jost B. and Kan, Haidong and Kanis, John A. and Kassebaum, Nicholas and Kawakami, Norito and Khang, Young Ho and Khatibzadeh, Shahab and Khoo, Jon Paul and Kok, Cindy and Laden, Francine and Lalloo, Ratilal and Lan, Qing and Lathlean, Tim and Leasher, Janet L. and Leigh, James and Li, Yang and Lin, John Kent and Lipshultz, Steven E. and London, Stephanie and Lozano, Rafael and Lu, Yuan and Mak, Joelle and Malekzadeh, Reza and Mallinger, Leslie and Marcenes, Wagner and March, Lyn and Marks, Robin and Martin, Randall and McGale, Paul and McGrath, John and Mehta, Sumi and Mensah, George A. and Merriman, Tony R. and Micha, Renata and Michaud, Catherine and Mishra, Vinod and Hanafiah, Khayriyyah Mohd and Mokdad, Ali A. and Morawska, Lidia and Mozaffarian, Dariush and Murphy, Tasha and Naghavi, Mohsen and Neal, Bruce and Nelson, Paul K. and Nolla, Joan Miquel and Norman, Rosana and Olives, Casey and Omer, Saad B. and Orchard, Jessica and Osborne, Richard and Ostro, Bart and Page, Andrew and Pandey, Kiran D. and Parry, Charles D H and Passmore, Erin and Patra, Jayadeep and Pearce, Neil and Pelizzari, Pamela M. and Petzold, Max and Phillips, Michael R. and Pope, Dan and Pope, C. Arden and Powles, John and Rao, Mayuree and Razavi, Homie and Rehfuess, Eva A. and Rehm, J{\"{u}}rgen T. and Ritz, Beate and Rivara, Frederick P. and Roberts, Thomas and Robinson, Carolyn and Rodriguez-Portales, Jose A. and Romieu, Isabelle and Room, Robin and Rosenfeld, Lisa C. and Roy, Ananya and Rushton, Lesley and Salomon, Joshua A. and Sampson, Uchechukwu and Sanchez-Riera, Lidia and Sanman, Ella and Sapkota, Amir and Seedat, Soraya and Shi, Peilin and Shield, Kevin and Shivakoti, Rupak and Singh, Gitanjali M. and Sleet, David A. and Smith, Emma and Smith, Kirk R. and Stapelberg, Nicolas J C and Steenland, Kyle and St{\"{o}}ckl, Heidi and Stovner, Lars Jacob and Straif, Kurt and Straney, Lahn and Thurston, George D. and Tran, Jimmy H. and {Van Dingenen}, Rita and {Van Donkelaar}, Aaron and Veerman, J. Lennert and Vijayakumar, Lakshmi and Weintraub, Robert and Weissman, Myrna M. and White, Richard A. and Whiteford, Harvey and Wiersma, Steven T. and Wilkinson, James D. and Williams, Hywel C. and Williams, Warwick and Wilson, Nicholas and Woolf, Anthony D. and Yip, Paul and Zielinski, Jan M. and Lopez, Alan D. and Murray, Christopher J L and Ezzati, Majid},
doi = {10.1016/S0140-6736(12)61766-8},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Lim et al. - 2012 - A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor cluste.pdf:pdf},
isbn = {0140-6736},
issn = {01406736},
journal = {Lancet},
keywords = {obesity},
mendeley-tags = {obesity},
number = {9859},
pages = {2224--2260},
pmid = {23245609},
title = {{A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: A systematic analysis for the Global Burden of Disease Study 2010}},
volume = {380},
year = {2012}
}
@article{Herzog1992,
abstract = {Neuropeptide Y (NPY) is one of the most abundant neuropeptides in the mammalian nervous system and exhibits a diverse range of important physiological activities, including effects on psychomotor activity, food intake, regulation of central endocrine secretion, and potent vasoactive effects on the cardiovascular system. Two major subtypes of NPY receptor (Y1 and Y2) have been defined by pharmacological criteria. We report here the molecular cloning of a cDNA sequence encoding a human NPY receptor and the corrected sequence for a rat homologue. Analysis of this sequence confirms that the receptor is a member of the G protein-coupled receptor superfamily. When expressed in Chinese hamster ovary (CHO) or human embryonic kidney (293) cells, the receptor exhibits the characteristic ligand specificity of a Y1 type of NPY receptor. In the 293 cell line, the receptor is coupled to a pertussis toxin-sensitive G protein that mediates the inhibition of cyclic AMP accumulation. In the CHO cell line, the receptor is coupled not to the inhibition of adenylate cyclase but rather to the elevation of intracellular calcium. These results demonstrate that second messenger coupling of the NPY-Y1 receptor is cell type specific, depending on the specific repertoire of G proteins and effector systems present in any cell type.},
author = {Herzog, H and Hort, Y J and Ball, H J and Hayes, G and Shine, J and Selbie, L A},
doi = {10.1073/pnas.89.13.5794},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Herzog et al. - 1992 - Cloned human neuropeptide Y receptor couples to two different second messenger systems.pdf:pdf},
isbn = {0027-8424 (Print)$\backslash$r0027-8424},
issn = {0027-8424},
journal = {Proc. Natl. Acad. Sci. U. S. A.},
keywords = {Adenylate Cyclase,Adenylate Cyclase: metabolism,Amino Acid Sequence,Base Sequence,Calcium,Calcium: metabolism,Cloning,DNA,DNA: genetics,Humans,Ligands,Molecular,Molecular Sequence Data,Neuropeptide Y,Neuropeptide Y: physiology,Neurotransmitter,Neurotransmitter: physiology,Receptors,Recombinant Proteins,Sequence Alignment,Signal Transduction,Transfection},
number = {13},
pages = {5794--5798},
pmid = {1321422},
title = {{Cloned human neuropeptide Y receptor couples to two different second messenger systems.}},
volume = {89},
year = {1992}
}
@article{Iodice2008,
author = {Iodice, Simona and Gandini, Sara and Maisonneuve, Patrick and Lowenfels, Albert B},
doi = {10.1007/s00423-007-0266-2},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Iodice et al. - 2008 - Tobacco and the risk of pancreatic cancer a review and meta-analysis.pdf:pdf},
keywords = {cancer,environmental factors,epidemiology,meta-analysis,pancreatic cancer,smoking,tobacco},
mendeley-tags = {cancer,environmental factors},
pages = {535--545},
title = {{Tobacco and the risk of pancreatic cancer : a review and meta-analysis}},
year = {2008}
}
@article{Vucenik2012,
abstract = {Obesity, a growing health problem worldwide, has been associated with the metabolic syndrome, diabetes, cardiovascular disease, hypertension, and other chronic diseases. Recently, the obesity-cancer link has received much attention. Epidemiological studies have shown that obesity is also associated with increased risk of several cancer types, including colon, breast, endometrium, liver, kidney, esophagus, gastric, pancreatic, gallbladder, and leukemia, and can also lead to poorer treatment and increased cancer-related mortality. Biological mechanisms underlying the relationship between obesity and cancer are not well understood. They include modulation of energy balance and calorie restriction, growth factors, multiple signaling pathways, and inflammatory processes. Key among the signaling pathways linking obesity and cancer is the PI3K/Akt/mTOR cascade, which is a target of many of the obesity-associated factors and regulates cell proliferation and survival. Understanding the molecular and cellular mechanisms of the obesity-cancer connection is important in developing potential therapeutics. The link between obesity and cancer underscores the recommendation to maintain a healthy body weight throughout life as one of the most important ways to protect against cancer.},
author = {Vucenik, Ivana and Stains, Joseph P.},
doi = {10.1111/j.1749-6632.2012.06750.x},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Vucenik, Stains - 2012 - Obesity and cancer risk Evidence, mechanisms, and recommendations.pdf:pdf},
isbn = {00778923 (ISSN)},
issn = {00778923},
journal = {Ann. N. Y. Acad. Sci.},
keywords = {Cancer,Mechanisms,Obesity,Prevention,Recommendations,obesity and cancer},
mendeley-tags = {obesity and cancer},
number = {1},
pages = {37--43},
pmid = {23050962},
title = {{Obesity and cancer risk: Evidence, mechanisms, and recommendations}},
volume = {1271},
year = {2012}
}
@book{Health2016b,
abstract = {An annual statistical publication that collates and analyses data on primary malignant tumour cases diagnosed in New Zealand, as reported to the New Zealand Cancer Registry.},
address = {Wellington},
author = {{New Zealand Ministry of Health}},
doi = {ISBN 978-0-478-3936-0},
file = {:Users/rikutakei/Downloads/papers/cancer-new-registrations-deaths-2013-nov16.pdf:pdf},
isbn = {9780478402827},
pages = {1--78},
pmid = {15608362},
publisher = {Ministry of Health},
title = {{Cancer : New registrations and deaths 2013}},
year = {2016}
}
@article{Friedman1998,
abstract = {The assimilation, storage and use of energy from nutrients constitute a homeostatic system that is essential for life. In vertebrates, the ability to store sufficient quantities of energy-dense triglyceride in adipose tissue allows survival during the frequent periods of food deprivation encountered during evolution. However, the presence of excess adipose tissue can be maladaptive. A complex physiological system has evolved to regulate fuel stores and energy balance at an optimum level. Leptin, a hormone secreted by adipose tissue, and its receptor are integral components of this system. Leptin also signals nutritional status to several other physiological systems and modulates their function. Here we review the role of leptin in the control of body weight and its relevance to the pathogenesis of obesity.},
author = {Friedman, J M and Halaas, J L},
doi = {10.1038/27376},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Friedman, Halaas - 1998 - Leptin and the regulation of body weight in mammals.pdf:pdf},
isbn = {0028-0836},
issn = {0028-0836},
journal = {Nature},
keywords = {obesity},
mendeley-tags = {obesity},
number = {6704},
pages = {763--770},
pmid = {9796811},
title = {{Leptin and the regulation of body weight in mammals.}},
volume = {395},
year = {1998}
}
@article{Guh2009,
abstract = {BACKGROUND: Overweight and obese persons are at risk of a number of medical conditions which can lead to further morbidity and mortality. The primary objective of this study is to provide an estimate of the incidence of each co-morbidity related to obesity and overweight using a meta-analysis.$\backslash$n$\backslash$nMETHODS: A literature search for the twenty co-morbidities identified in a preliminary search was conducted in Medline and Embase (Jan 2007). Studies meeting the inclusion criteria (prospective cohort studies of sufficient size reporting risk estimate based on the incidence of disease) were extracted. Study-specific unadjusted relative risks (RRs) on the log scale comparing overweight with normal and obese with normal were weighted by the inverse of their corresponding variances to obtain a pooled RR with 95{\%} confidence intervals (CI).$\backslash$n$\backslash$nRESULTS: A total of 89 relevant studies were identified. The review found evidence for 18 co-morbidities which met the inclusion criteria. The meta-analysis determined statistically significant associations for overweight with the incidence of type II diabetes, all cancers except esophageal (female), pancreatic and prostate cancer, all cardiovascular diseases (except congestive heart failure), asthma, gallbladder disease, osteoarthritis and chronic back pain. We noted the strongest association between overweight defined by body mass index (BMI) and the incidence of type II diabetes in females (RR = 3.92 (95{\%} CI: 3.10-4.97)). Statistically significant associations with obesity were found with the incidence of type II diabetes, all cancers except esophageal and prostate cancer, all cardiovascular diseases, asthma, gallbladder disease, osteoarthritis and chronic back pain. Obesity defined by BMI was also most strongly associated with the incidence of type II diabetes in females (12.41 (9.03-17.06)).$\backslash$n$\backslash$nCONCLUSION: Both overweight and obesity are associated with the incidence of multiple co-morbidities including type II diabetes, cancer and cardiovascular diseases. Maintenance of a healthy weight could be important in the prevention of the large disease burden in the future. Further studies are needed to explore the biological mechanisms that link overweight and obesity with these co-morbidities.},
author = {Guh, Daphne P and Zhang, Wei and Bansback, Nick and Amarsi, Zubin and Birmingham, C Laird and Anis, Aslam H},
doi = {10.1186/1471-2458-9-88},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Guh et al. - 2009 - The incidence of co-morbidities related to obesity and overweight a systematic review and meta-analysis.pdf:pdf},
isbn = {1471-2458 (Electronic)$\backslash$n1471-2458 (Linking)},
issn = {1471-2458},
journal = {BMC Public Health},
keywords = {Cardiovascular Diseases,Cardiovascular Diseases: epidemiology,Comorbidity,Diabetes Mellitus,Female,Gallbladder Diseases,Gallbladder Diseases: epidemiology,Humans,Incidence,Male,Neoplasms,Neoplasms: epidemiology,Obesity,Obesity: epidemiology,Osteoarthritis,Osteoarthritis: epidemiology,Overweight,Overweight: epidemiology,Type 2,Type 2: epidemiology,obesity risk},
mendeley-tags = {obesity risk},
pages = {88},
pmid = {19320986},
title = {{The incidence of co-morbidities related to obesity and overweight: a systematic review and meta-analysis.}},
volume = {9},
year = {2009}
}
@article{Fuqua1991,
author = {Fuqua, SAW and Fitzgerald, SD and Chamness, GC},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Fuqua, Fitzgerald, Chamness - 1991 - Variant human breast tumor estrogen receptor with constitutive transcriptional activity.pdf:pdf},
journal = {Cancer Res.},
keywords = {cancer},
mendeley-tags = {cancer},
number = {14},
pages = {105--109},
title = {{Variant human breast tumor estrogen receptor with constitutive transcriptional activity}},
volume = {8},
year = {1991}
}
@article{Dina2007,
abstract = {We identified a set of SNPs in the first intron of the FTO (fat mass and obesity associated) gene on chromosome 16q12.2 that is consistently strongly associated with early-onset and severe obesity in both adults and children of European ancestry with an experiment-wise P value of 1.67 x 10(-26) in 2,900 affected individuals and 5,100 controls. The at-risk haplotype yields a proportion of attributable risk of 22{\%} for common obesity. We conclude that FTO contributes to human obesity and hence may be a target for subsequent functional analyses.},
author = {Dina, Christian and Meyre, David and Gallina, Sophie and Durand, Emmanuelle and K{\"{o}}rner, Antje and Jacobson, Peter and Carlsson, Lena M S and Kiess, Wieland and Vatin, Vincent and Lecoeur, Cecile and Delplanque, J{\'{e}}rome and Vaillant, Emmanuel and Pattou, Fran{\c{c}}ois and Ruiz, Juan and Weill, Jacques and Levy-Marchal, Claire and Horber, Fritz and Potoczna, Natascha and Hercberg, Serge and {Le Stunff}, Catherine and Bougn{\`{e}}res, Pierre and Kovacs, Peter and Marre, Michel and Balkau, Beverley and Cauchi, St{\'{e}}phane and Ch{\`{e}}vre, Jean-Claude and Froguel, Philippe},
doi = {10.1038/ng2048},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Dina et al. - 2007 - Variation in FTO contributes to childhood obesity and severe adult obesity.pdf:pdf},
isbn = {1061-4036 (Print)$\backslash$n1061-4036 (Linking)},
issn = {1061-4036},
journal = {Nat. Genet.},
keywords = {Adiposity,Adult,Age of Onset,Body Composition,Body Mass Index,Case-Control Studies,Child,Chromosomes, Human, Pair 16,Chromosomes, Human, Pair 16: genetics,Cohort Studies,Europe,FTO,Female,GWAS,Genetic Predisposition to Disease,Genetic Variation,Genetic Variation: genetics,Human,Humans,Introns,Introns: genetics,Male,Middle Aged,Obesity,Obesity: genetics,Pair 16,Pair 16: genetics,Polymorphism, Single Nucleotide,Polymorphism, Single Nucleotide: genetics,Single Nucleotide,Single Nucleotide: genetics,obesity},
mendeley-tags = {FTO,GWAS,obesity},
number = {6},
pages = {724--726},
pmid = {17496892},
title = {{Variation in FTO contributes to childhood obesity and severe adult obesity.}},
volume = {39},
year = {2007}
}
@article{Holder2000,
abstract = {Studies of mice and humans have revealed a number of genes that when mutated result in severe obesity. We have studied a unique girl with early-onset obesity and a de novo balanced translocation between chromosomes 1p22.1 and 6q16.2. Her weight gain is most likely due to excessive food intake, since measured energy expenditure was normal. We cloned and sequenced both translocation breakpoints. The translocation does not appear to affect any transcription unit on 1p, but it disrupts the SIM1 gene on 6q. SIM1 encodes a human homolog of Drosophila Sim (Single-minded), a transcription factor involved in midline neurogenesis, and is a prototypical member of the bHLH-PAS (basic helix-loop-helix + period, aryl hydrocarbon receptor, Single-minded) gene family. Our subject's trans- location separates the 5' promoter region and bHLH domain from the 3' PAS and putative transcriptional regulation domains. The transcriptional targets of SIM1 are not known. Mouse Sim1 is expressed in the developing kidney and central nervous system, and is essential for formation of the supraoptic and paraventricular (PVN) nuclei of the hypothalamus. Previous neuroanatomical and pharmacological studies have implicated the PVN in the regulation of body weight: PVN neurons express the melanocortin 4 receptor and appear to be physiological targets of alpha-melanocyte-stimulating hormone, which inhibits food intake. We hypothesize that haploinsufficiency of SIM1, possibly acting upstream or downstream of the melanocortin 4 receptor in the PVN, is responsible for severe obesity in our subject.},
author = {Holder, J L and Butte, N F and Zinn, a R},
doi = {ddd012 [pii]},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Holder, Butte, Zinn - 2000 - Profound obesity associated with a balanced translocation that disrupts the SIM1 gene.pdf:pdf},
isbn = {0964-6906},
issn = {0964-6906},
journal = {Hum. Mol. Genet.},
keywords = {obesity},
mendeley-tags = {obesity},
number = {1},
pages = {101--108},
pmid = {10587584},
title = {{Profound obesity associated with a balanced translocation that disrupts the SIM1 gene.}},
volume = {9},
year = {2000}
}
@article{Khatri2005,
abstract = {Independent of the platform and the analysis methods used, the result of a microarray experiment is, in most cases, a list of differentially expressed genes. An automatic ontological analysis approach has been recently proposed to help with the biological interpretation of such results. Currently, this approach is the de facto standard for the secondary analysis of high throughput experiments and a large number of tools have been developed for this purpose. We present a detailed comparison of 14 such tools using the following criteria: scope of the analysis, visualization capabilities, statistical model(s) used, correction for multiple comparisons, reference microarrays available, installation issues and sources of annotation data. This detailed analysis of the capabilities of these tools will help researchers choose the most appropriate tool for a given type of analysis. More importantly, in spite of the fact that this type of analysis has been generally adopted, this approach has several important intrinsic drawbacks. These drawbacks are associated with all tools discussed and represent conceptual limitations of the current state-of-the-art in ontological analysis. We propose these as challenges for the next generation of secondary data analysis tools.},
archivePrefix = {arXiv},
arxivId = {NIHMS150003},
author = {Khatri, Purvesh and Drǎghici, Sorin},
doi = {10.1093/bioinformatics/bti565},
eprint = {NIHMS150003},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Khatri, Drǎghici - 2005 - Ontological analysis of gene expression data Current tools, limitations, and open problems.pdf:pdf},
isbn = {1367-4803 (Print)$\backslash$r1367-4803 (Linking)},
issn = {13674803},
journal = {Bioinformatics},
number = {18},
pages = {3587--3595},
pmid = {15994189},
title = {{Ontological analysis of gene expression data: Current tools, limitations, and open problems}},
volume = {21},
year = {2005}
}
@article{Schena1995,
abstract = {A high-capacity system was developed to monitor the expression of many genes in parallel. Microarrays prepared by high-speed robotic printing of complementary DNAs on glass were used for quantitative expression measurements of the corresponding genes. Because of the small format and high density of the arrays, hybridization volumes of 2 microliters could be used that enabled detection of rare transcripts in probe mixtures derived from 2 micrograms of total cellular messenger RNA. Differential expression measurements of 45 Arabidopsis genes were made by means of simultaneous, two-color fluorescence hybridization.},
author = {Schena, Mark and Shalon, Dari and Davis, Ronald W. and Brown, Patrick O.},
doi = {10.1126/science.270.5235.467},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Schena et al. - 1995 - Quantitative monitoring of gene expression patterns with a complementary DNA microarray.pdf:pdf},
isbn = {0036-8075},
issn = {0036-8075},
journal = {Science (80-. ).},
number = {5235},
pages = {467--470},
pmid = {7569999},
title = {{Quantitative monitoring of gene expression patterns with a complementary DNA microarray}},
volume = {270},
year = {1995}
}
@article{Koppenol2011,
abstract = {Otto Warburg pioneered quantitative investigations of cancer cell metabolism, as well as photosynthesis and respiration. Warburg and co-workers showed in the 1920s that, under aerobic conditions, tumour tissues metabolize approximately tenfold more glucose to lactate in a given time than normal tissues, a phenomenon known as the Warburg effect. However, this increase in aerobic glycolysis in cancer cells is often erroneously thought to occur instead of mitochondrial respiration and has been misinterpreted as evidence for damage to respiration instead of damage to the regulation of glycolysis. In fact, many cancers exhibit the Warburg effect while retaining mitochondrial respiration. We re-examine Warburg's observations in relation to the current concepts of cancer metabolism as being intimately linked to alterations of mitochondrial DNA, oncogenes and tumour suppressors, and thus readily exploitable for cancer therapy.},
author = {Koppenol, Willem H and Bounds, Patricia L and Dang, Chi V},
doi = {10.1038/nrc3038},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Koppenol, Bounds, Dang - 2011 - Otto Warburg's contributions to current concepts of cancer metabolism.pdf:pdf},
isbn = {1474-1768 (Electronic)$\backslash$r1474-175X (Linking)},
issn = {1474-1768},
journal = {Nat. Rev. Cancer},
keywords = {20th Century,Cell Respiration,Cell Respiration: physiology,Germany,Glycolysis,Glycolysis: physiology,History,Humans,Neoplasms,Neoplasms: history,Neoplasms: metabolism,Neoplasms: pathology,cancer,energy},
mendeley-tags = {cancer,energy},
number = {5},
pages = {325--37},
pmid = {21508971},
title = {{Otto Warburg's contributions to current concepts of cancer metabolism.}},
volume = {11},
year = {2011}
}
@article{Hoeijmakers2001,
abstract = {The early notion that cancer is caused by mutations in genes critical for the control of cell growth implied that genome stability is important for preventing oncogenesis. During the past decade, knowledge about the mechanisms by which genes erode and the molecular machinery designed to counteract this time-dependent genetic degeneration has increased markedly. At the same time, it has become apparent that inherited or acquired deficiencies in genome maintenance systems contribute significantly to the onset of cancer. This review summarizes the main DNA caretaking systems and their impact on genome stability and carcinogenesis.},
author = {Hoeijmakers, Jan H J},
doi = {10.1038/35077232},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Hoeijmakers - 2001 - Genome maintenance mechanisms for preventing cancer.pdf:pdf},
isbn = {0028-0836 (Print)},
issn = {00280836},
journal = {Nature},
keywords = {cancer,environmental factors},
mendeley-tags = {cancer,environmental factors},
pages = {366--374},
pmid = {11357144},
title = {{Genome maintenance mechanisms for preventing cancer}},
volume = {411},
year = {2001}
}
@article{WHO2006,
abstract = {30 p.},
author = {{World Health Organisation}},
doi = {10.1007/SpringerReference_301104},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/World Health Organisation - 2006 - Global strategy on diet, physical activity and health a framework to monitor and evaluate implementat.pdf:pdf},
isbn = {ISBN 978 92 4 159454 7},
issn = {1467-789X},
journal = {Geneva World Heal. Organ.},
title = {{Global strategy on diet, physical activity and health: a framework to monitor and evaluate implementation}},
year = {2006}
}
@article{Vogelstein2004a,
abstract = {The revolution in cancer research can be summed up in a single sentence: cancer is, in essence, a genetic disease. In the last decade, many important genes responsible for the genesis of various cancers have been discovered, their mutations precisely identified, and the pathways through which they act characterized. The purposes of this review are to highlight examples of progress in these areas, indicate where knowledge is scarce and point out fertile grounds for future investigation.},
author = {Vogelstein, B and Kinzler, K},
doi = {10.1038/nm1087},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Vogelstein, Kinzler - 2004 - Cancer genes and the pathways they control.pdf:pdf},
isbn = {1078-8956},
issn = {10788956},
journal = {Nat. Med.},
keywords = {1-Phosphatidylinositol 3-Kinase,Adenomatous Polyposis Coli Protein,Apoptosis,DNA Repair,DNA-Binding Proteins,Genes: Tumor Suppressor,Humans,Hypoxia-Inducible Factor 1,Hypoxia-Inducible Factor 1: alpha Subunit,Mutation,Neoplasms,Nuclear Proteins,Oncogenes,Receptor Protein-Tyrosine Kinases,Retinoblastoma Protein,Signal Transduction,Smad Proteins,Trans-Activators,Transcription Factors,Tumor Suppressor Protein p53,cancer,genes and mutations,review},
mendeley-tags = {cancer,genes and mutations,review},
number = {8},
pages = {789--799},
pmid = {15286780},
title = {{Cancer genes and the pathways they control}},
volume = {10},
year = {2004}
}
@article{Gatza2010a,
abstract = {The hallmark of human cancer is heterogeneity, reflecting the complexity and variability of the vast array of somatic mutations acquired during oncogenesis. An ability to dissect this heterogeneity, to identify subgroups that represent common mechanisms of disease, will be critical to understanding the complexities of genetic alterations and to provide a framework to develop rational therapeutic strategies. Here, we describe a classification scheme for human breast cancer making use of patterns of pathway activity to build on previous subtype characterizations using intrinsic gene expression signatures, to provide a functional interpretation of the gene expression data that can be linked to therapeutic options. We show that the identified subgroups provide a robust mechanism for classifying independent samples, identifying tumors that share patterns of pathway activity and exhibit similar clinical and biological properties, including distinct patterns of chromosomal alterations that were not evident in the heterogeneous total population of tumors. We propose that this classification scheme provides a basis for understanding the complex mechanisms of oncogenesis that give rise to these tumors and to identify rational opportunities for combination therapies.},
author = {Gatza, Michael L and Lucas, Joseph E and Barry, William T and Kim, Jong Wook and Wang, Quanli and Crawford, Matthew D and Datto, Michael B and Kelley, Michael and Mathey-Prevot, Bernard and Potti, Anil and Nevins, Joseph R},
doi = {10.1073/pnas.0912708107},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Gatza et al.{\_}2010{\_}A pathway-based classification of human breast cancer.pdf:pdf},
isbn = {0912708107},
issn = {1091-6490},
journal = {Proc. Natl. Acad. Sci. U. S. A.},
keywords = {Key Paper},
mendeley-tags = {Key Paper},
number = {15},
pages = {6994--6999},
pmid = {20335537},
title = {{A pathway-based classification of human breast cancer.}},
volume = {107},
year = {2010}
}
@article{Albuquerque2015,
abstract = {It is well-known that obesity is a complex multifactorial and heterogeneous condition with an important genetic component. Recently, major advances in obesity research emerged concerning the molecular mechanisms contributing to the obese condition. This review outlines several studies and data concerning the genetics and other important factors in the susceptibility risk to develop obesity. Based in the genetic etiology three main categories of obesity are considered: monogenic, syndromic, and common obesity. For the monogenic forms of obesity, the gene causing the phenotype is clearly identified, whereas for the common obesity the loci architecture underlying the phenotype is still being characterized. Given that, in this review we focus mainly in this obesity form, reviewing loci found until now by genome-wide association studies related with the susceptibility risk to develop obesity. Moreover, we also detail the obesity-related loci identified in children and in different ethnic groups, trying to highlight the complexity of the genetics underlying the common obese phenotype. Importantly, we also focus in the evolutionary hypotheses that have been proposed trying to explain how natural selection favored the spread of genes that increase the risk for an obese phenotype and how this predisposition to obesity evolved. Other factors are important in the obesity condition, and thus, we also discuss the epigenetic mechanisms involved in the susceptibility and development of obesity. Covering all these topics we expect to provide a complete and recent perspective about the underlying mechanisms involved in the development and origin of obesity. Only with a full understanding of the factors and mechanisms contributing to obesity, it will be possible to provide and allow the development of new therapeutic approaches to this condition.},
author = {Albuquerque, David and Stice, Eric and Rodr{\'{i}}guez-L{\'{o}}pez, Raquel and Manco, Lic{\'{i}}no and N{\'{o}}brega, Cl{\'{e}}vio},
doi = {10.1007/s00438-015-1015-9},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Albuquerque et al. - 2015 - Current review of genetics of human obesity from molecular mechanisms to an evolutionary perspective.pdf:pdf},
isbn = {1617-4615},
issn = {16174623},
journal = {Mol. Genet. Genomics},
keywords = {Epigenetics,Evolutionary perspectives,Genetics of obesity,MicroRNAs,Nutrigenomics,Obesity,obesity},
mendeley-tags = {obesity},
pages = {1191--1221},
pmid = {25749980},
publisher = {Springer Berlin Heidelberg},
title = {{Current review of genetics of human obesity: from molecular mechanisms to an evolutionary perspective}},
volume = {290},
year = {2015}
}
@article{Kohno2003,
author = {Kohno, Daisuke and Gao, Hong-zhi and Muroya, Shinji and Kikuyama, Sakae and Yada, Toshihiko},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Kohno et al. - 2003 - Ghrelin directly interacts with neuropeptide-Y-containing neurons in the rat arcuate nucleus Ca2 signaling via pro.pdf:pdf},
journal = {Diabetes},
keywords = {obesity},
mendeley-tags = {obesity},
pages = {948--956},
title = {{Ghrelin directly interacts with neuropeptide-Y-containing neurons in the rat arcuate nucleus: Ca2+ signaling via protein kinase A and N-type channel-dependent mechanisms and cross-talk with leptin and orexin}},
volume = {52},
year = {2003}
}
@article{Saxena2006,
abstract = {Obesity, as a core component of the metabolic syndrome, is among the top ten global health risks classified by the World Health Organization (WHO) as being strongly associated with the development and progression of chronic renal disease--a widely prevalent but often silent condition. Obesity carries elevated risks of cardiovascular morbidity and mortality besides having an array of metabolic complications. Maladaptive glomerular hemodynamics with increased intraglomerular pressure in association with vasoactive, fibrogenic substances released from adipocytes, in addition to cytokines and hormones, are the key factors in the causation of renal injury and the progression of nephron loss among obese subjects.},
author = {Saxena, Anil Kumar},
doi = {10.1093/epirev/mxm012},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Saxena - 2006 - Emerging global epidemic of obesity The renal perspective.pdf:pdf},
isbn = {0256-4947 (Print)$\backslash$n0256-4947 (Linking)},
issn = {02564947},
journal = {Ann. Saudi Med.},
keywords = {obesity},
mendeley-tags = {obesity},
number = {4},
pages = {288--295},
pmid = {16883080},
title = {{Emerging global epidemic of obesity: The renal perspective}},
volume = {26},
year = {2006}
}
@article{Jarde2011,
abstract = {Obesity is associated with an increased risk of breast cancer in postmenopausal women. Accumulating evidence suggests that adipose tissue, which is an endocrine organ producing a large range of factors, may interfere with breast cancer development. Leptin and adiponectin are two major adipocyte-secreted hormones. The pro-carcinogenic effect of leptin and conversely, the anti-carcinogenic effect of adiponectin result from two main mechanisms: a modulation in the signalling pathways involved in proliferation process and a subtle regulation of the apoptotic response. This review provides insight into recent findings on the molecular mechanisms of leptin and adiponectin in mammary tumours, and discusses the potential interplay between these two adipokines in breast cancer.},
author = {Jard{\'{e}}, Thierry and Perrier, St{\'{e}}phane and Vasson, Marie-Paule and Caldefie-Ch{\'{e}}zet, Florence},
doi = {10.1016/j.ejca.2010.09.005},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Jard{\'{e}} et al. - 2011 - Molecular mechanisms of leptin and adiponectin in breast cancer.pdf:pdf},
isbn = {1879-0852 (Electronic)$\backslash$r0959-8049 (Linking)},
issn = {09598049},
journal = {Eur. J. Cancer},
number = {1},
pages = {33--43},
pmid = {20889333},
title = {{Molecular mechanisms of leptin and adiponectin in breast cancer.}},
volume = {47},
year = {2011}
}
@article{Benjamini1995a,
author = {Benjamini, Yoav and Hochberg, Yosef},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Benjamini, Hochberg - 1995 - Controlling the False Discovery Rate A Practical and Powerful Approach to Multiple Testing.pdf:pdf},
journal = {J. R. Stat. Soc. Ser. B},
number = {1},
pages = {289--300},
title = {{Controlling the False Discovery Rate : A Practical and Powerful Approach to Multiple Testing}},
volume = {57},
year = {1995}
}
@article{Smith1988,
abstract = {Introduction More than 20 yr ago, in an elegant series of pulsechase studies, Steiner and Oyer (1) demonstrated that insulin is synthesized in pancreatic islet cells as part of a larger molecule, proinsulin. Since that time, the concept that bioactive peptides are derived from larger precursors has become firmly established (2–4). Over the same period, the definitive structures of the majority of precursors of biologically active peptides have been fully characterized, both by classical protein sequence studies and more recently by recombinant DNA techniques (for reviews see Refs. 4–6). To yield biologically active products, precursors commonly undergo a series of highly organized posttranslational events, including selective proteolytic cleavage and other enzymatic modifications (e.g., phosphorylation, $\alpha$-amidation, acetylation) which take place within specific membrane-bounded compartments. A number of precursor polypeptides contain within their structure amino acid sequences which have quite diverse bio...},
author = {Smith, A. I. and Funder, J. W.},
doi = {10.1210/edrv-9-1-159},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Smith, Funder - 1988 - Proopiomelanocortin processing in the pituitary, central nervous system, and peripheral tissues.pdf:pdf},
isbn = {10.1210/edrv-9-1-159},
issn = {0163769X},
journal = {Endocr. Rev.},
number = {1},
pages = {159--179},
pmid = {3286233},
title = {{Proopiomelanocortin processing in the pituitary, central nervous system, and peripheral tissues.}},
volume = {9},
year = {1988}
}
@article{Rogge2008,
abstract = {Over the past decade or so, CART (cocaine- and amphetamine-regulated transcript) peptides have emerged as major neurotransmitters and hormones. CART peptides are widely distributed in the CNS and are involved in regulating many processes, including food intake and the maintenance of body weight, reward and endocrine functions. Recent studies have produced a wealth of information about the location, regulation, processing and functions of CART peptides, but additional studies aimed at elucidating the physiological effects of the peptides and at characterizing the CART receptor(s) are needed to take advantage of possible therapeutic applications.},
author = {Rogge, G and Jones, D and Hubert, G W and Lin, Y and Kuhar, M J},
doi = {10.1038/nrn2493},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Rogge et al. - 2008 - CART peptides regulators of body weight, reward and other functions.pdf:pdf},
isbn = {1471-003X},
issn = {1471-0048},
journal = {Nat. Rev. Neurosci.},
keywords = {Affective Symptoms,Affective Symptoms: genetics,Affective Symptoms: metabolism,Affective Symptoms: physiopathology,Animals,Appetite Regulation,Appetite Regulation: physiology,Body Weight,Body Weight: physiology,Cell Surface,Cell Surface: metabolism,Central Nervous System,Central Nervous System: anatomy {\&} histology,Central Nervous System: metabolism,Humans,Messenger,Messenger: genetics,Messenger: metabolism,Nerve Tissue Proteins,Nerve Tissue Proteins: genetics,Nerve Tissue Proteins: metabolism,RNA,Receptors,Reward,Signal Transduction,Signal Transduction: physiology},
number = {10},
pages = {747--758},
pmid = {18802445},
title = {{CART peptides: regulators of body weight, reward and other functions}},
volume = {9},
year = {2008}
}
@article{Prives1999,
abstract = {Abnormalities of the p53 tumour suppressor gene are among the most frequent molecular events in human and animal neoplasia. Moreover, p53 is one of the most studied proteins in the whole of contemporary biology, with more than 12,500 papers so far written! In this review the choice has been deliberately made not to be fully comprehensive in the coverage of the huge p53 literature. Rather attention is focused on a small number of recent developments which are reviewed in the context of modern models of p53 function. Progress in the analysis of signalling to p53 including phosphorylation cascades, and interactions with proteins such as mdm2 and ARF are highlighted. The plethora of protein-protein interactions is discussed, as are the strategies for defining downstream targets of p53. Finally, the emerging biology of p53 homologues is considered. The need for bridging the gap between reductionist, biochemical and biophysical studies and biological and genetic analysis is emphasized. Only this will provide the needed framework for utilizing the information in clinical care.},
author = {Prives, C and Hall, P A},
doi = {10.1002/(SICI)1096-9896(199901)187:1<112::AID-PATH250>3.0.CO;2-3},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Prives, Hall - 1999 - The p53 pathway.pdf:pdf},
isbn = {0022-3417},
issn = {0022-3417},
journal = {J. Pathol.},
keywords = {Animals,Humans,Neoplasm Proteins,Neoplasm Proteins: physiology,Neoplasms,Neoplasms: genetics,Neoplasms: physiopathology,Phosphorylation,Signal Transduction,Tumor Suppressor Protein p53,Tumor Suppressor Protein p53: physiology,cancer,p53},
mendeley-tags = {cancer,p53},
number = {1},
pages = {112--126},
pmid = {10341712},
title = {{The p53 pathway}},
volume = {187},
year = {1999}
}
@article{Friedberg2003,
author = {Friedberg, Errol C},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Friedberg - 2003 - DNA damage and repair.pdf:pdf},
journal = {Nature},
keywords = {cancer,environmental factors},
mendeley-tags = {cancer,environmental factors},
pages = {436--440},
title = {{DNA damage and repair}},
volume = {421},
year = {2003}
}
@article{Armstrong1975,
abstract = {Incidence rates for 27 cancers in 23 countries and mortality rates for 14 cancers in 32 countries have been correlated with a wide range of dietary and other variables. Dietary variables were strongly correlated with several types of cancer, particularly meat consumption with cancer of the colon and fat consumption with cancers of the breast and corpus uteri. The data suggest a possible role for dietary factors in modifying the development of cancer at a number of other sites. The usefulness and limitations of the method are discussed.},
author = {Armstrong, B B and Doll, R R},
doi = {10.1002/ijc.2910150411},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Armstrong, Doll - 1975 - Environmental factors and cancer incidence and mortality in different countries, with special reference to diet.pdf:pdf},
isbn = {1097-0215},
issn = {0020-7136},
journal = {Int. J. Cancer},
keywords = {cancer,environmental factors},
mendeley-tags = {cancer,environmental factors},
number = {4},
pages = {617--631},
pmid = {1140864},
title = {{Environmental factors and cancer incidence and mortality in different countries, with special reference to dietary practices.}},
volume = {15},
year = {1975}
}
@article{Alexandrov2013,
abstract = {All cancers are caused by somatic mutations; however, understanding of the biological processes generating these mutations is limited. The catalogue of somatic mutations from a cancer genome bears the signatures of the mutational processes that have been operative. Here we analysed 4,938,362 mutations from 7,042 cancers and extracted more than 20 distinct mutational signatures. Some are present in many cancer types, notably a signature attributed to the APOBEC family of cytidine deaminases, whereas others are confined to a single cancer class. Certain signatures are associated with age of the patient at cancer diagnosis, known mutagenic exposures or defects in DNA maintenance, but many are of cryptic origin. In addition to these genome-wide mutational signatures, hypermutation localized to small genomic regions, 'kataegis', is found in many cancer types. The results reveal the diversity of mutational processes underlying the development of cancer, with potential implications for understanding of cancer aetiology, prevention and therapy.},
author = {Alexandrov, Ludmil B and Nik-Zainal, Serena and Wedge, David C and Aparicio, Samuel A J R and Behjati, Sam and Biankin, Andrew V and Bignell, Graham R and Bolli, Niccol{\`{o}} and Borg, Ake and B{\o}rresen-Dale, Anne-Lise and Boyault, Sandrine and Burkhardt, Birgit and Butler, Adam P and Caldas, Carlos and Davies, Helen R and Desmedt, Christine and Eils, Roland and Eyfj{\"{o}}rd, J{\'{o}}runn Erla and Foekens, John a and Greaves, Mel and Hosoda, Fumie and Hutter, Barbara and Ilicic, Tomislav and Imbeaud, Sandrine and Imielinski, Marcin and Imielinsk, Marcin and J{\"{a}}ger, Natalie and Jones, David T W and Jones, David and Knappskog, Stian and Kool, Marcel and Lakhani, Sunil R and L{\'{o}}pez-Ot{\'{i}}n, Carlos and Martin, Sancha and Munshi, Nikhil C and Nakamura, Hiromi and Northcott, Paul a and Pajic, Marina and Papaemmanuil, Elli and Paradiso, Angelo and Pearson, John V and Puente, Xose S and Raine, Keiran and Ramakrishna, Manasa and Richardson, Andrea L and Richter, Julia and Rosenstiel, Philip and Schlesner, Matthias and Schumacher, Ton N and Span, Paul N and Teague, Jon W and Totoki, Yasushi and Tutt, Andrew N J and Vald{\'{e}}s-Mas, Rafael and van Buuren, Marit M and {van 't Veer}, Laura and Vincent-Salomon, Anne and Waddell, Nicola and Yates, Lucy R and Zucman-Rossi, Jessica and Futreal, P Andrew and McDermott, Ultan and Lichter, Peter and Meyerson, Matthew and Grimmond, Sean M and Siebert, Reiner and Campo, El{\'{i}}as and Shibata, Tatsuhiro and Pfister, Stefan M and Campbell, Peter J and Stratton, Michael R},
doi = {10.1038/nature12477},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Alexandrov et al.{\_}2013{\_}Signatures of mutational processes in human cancer.pdf:pdf},
isbn = {1476-4687 (Electronic)$\backslash$r0028-0836 (Linking)},
issn = {1476-4687},
journal = {Nature},
keywords = {Aging,Aging: genetics,Algorithms,Cell Transformation,Cytidine Deaminase,Cytidine Deaminase: genetics,DNA,DNA Mutational Analysis,DNA: genetics,DNA: metabolism,Genetic,Genetic: genetics,Humans,Insertional,Insertional: genetics,Models,Mutagenesis,Mutagenesis: genetics,Mutagens,Mutagens: pharmacology,Mutation,Mutation: genetics,Neoplasms,Neoplasms: enzymology,Neoplasms: genetics,Neoplasms: pathology,Neoplastic,Neoplastic: genetics,Neoplastic: pathology,Organ Specificity,Reproducibility of Results,Sequence Deletion,Sequence Deletion: genetics,Transcription},
number = {7463},
pages = {415--421},
pmid = {23945592},
title = {{Signatures of mutational processes in human cancer.}},
volume = {500},
year = {2013}
}
@article{Liotta2001,
abstract = {Throughout the entire process of cancer aetiology, progression and metastasis, the microenvironment of the local host tissue can be an active participant. Invasion occurs within a tumour-host microecology, where stroma and tumour cells exchange enzymes and cytokines that modify the local extracellular matrix, stimulate migration, and promote proliferation and survival. A new class of cancer therapies that targets this pathological communication interface between tumour cells and host cells is currently under development.},
author = {Liotta, L A and Kohn, E C},
doi = {10.1038/35077241},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Liotta, Kohn - 2001 - The microenvironment of the tumour-host interface.pdf:pdf},
isbn = {0028-0836 (Print)$\backslash$r0028-0836 (Linking)},
issn = {0028-0836},
journal = {Nature},
keywords = {cancer},
mendeley-tags = {cancer},
number = {6835},
pages = {375--379},
pmid = {11357145},
title = {{The microenvironment of the tumour-host interface.}},
volume = {411},
year = {2001}
}
@article{Mantovani2008,
author = {Mantovani, Alberto and Allavena, Paola and Sica, Antonio and Balkwill, Frances},
doi = {10.1038/nature07205},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Mantovani et al. - 2008 - Cancer-related inflammation.pdf:pdf},
isbn = {1476-4687; 0028-0836},
issn = {0028-0836},
journal = {Nature},
keywords = {cancer,inflammation},
mendeley-tags = {cancer,inflammation},
number = {7203},
pages = {436--444},
pmid = {2008472523},
title = {{Cancer-related inflammation}},
volume = {454},
year = {2008}
}
@article{Kublaoui2006,
abstract = {Single-minded 1 (SIM1) mutations are associated with obesity in mice and humans. Haploinsufficiency of mouse Sim1 causes hyperphagic obesity with increased linear growth and enhanced sensitivity to a high-fat diet, a phenotype similar to that of agouti yellow and melanocortin 4 receptor knockout mice. To investigate the effects of increased Sim1 dosage, we generated transgenic mice that overexpress human SIM1 and examined their phenotype. Compared with wild-type mice, SIM1 transgenic mice had no obvious phenotype on a low-fat chow diet but were resistant to diet-induced obesity on a high-fat diet due to reduced food intake with no change in energy expenditure. The SIM1 transgene also completely rescued the hyperphagia and partially rescued the obesity of agouti yellow mice, in which melanocortin signaling is abrogated. Our results indicate that the melanocortin 4 receptor signals through Sim1 or its transcriptional targets in controlling food intake but not energy expenditure.},
author = {Kublaoui, Bassil M. and Holder, J. Lloyd and Tolson, Kristen P. and Gemelli, Terry and Zinn, Andrew R.},
doi = {10.1210/en.2006-0453},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Kublaoui et al. - 2006 - SIM1 overexpression partially rescues agouti yellow and diet-induced obesity by normalizing food intake.pdf:pdf},
isbn = {0013-7227 (Print)$\backslash$r0013-7227 (Linking)},
issn = {00137227},
journal = {Endocrinology},
keywords = {obesity},
mendeley-tags = {obesity},
number = {10},
pages = {4542--4549},
pmid = {16709610},
title = {{SIM1 overexpression partially rescues agouti yellow and diet-induced obesity by normalizing food intake}},
volume = {147},
year = {2006}
}
@article{Woods1979,
abstract = {Body adiposity is normally maintained within rigid limits. Although it is not clear that this regulation fits a strict negative feedback pattern, animals do maintain a relatively constant body adiposity. It has been postulated that this regulation is mediated by some signal which informs centres controlling food intake, probably located in the brain, as to the present state of adiposity. The identity of the signal is unknown, but the direct correlation between body adiposity and basal insulin levels in the plasma, suggests insulin as a possible candidate. This hormone is present in the cerbrospinal fluid (CSF) of many species, and is a slow integral over time of the level within the plasma. Thus, the level of insulin in the CSF is relatively resistant to short-term plasma fluctuations of insulin. Obese humans have higher levels of CSF insulin than lean controls and the CSF insulin level of both obese and lean humans is reduced proportionately after a prolonged fast. We have therefore postulated that the feedback system responding to body adiposity uses the concentration of insulin in the CSF as a major signal. Additional support for such a role is found in recent reports that insulin receptors are present in several regions of the brain and spinal cord. We now present additional evidence for our hypothesis by showing that in baboons the infusion of exogenous insulin into the CSF elicits a reliable and predictable decrease in food intake and body weight.},
archivePrefix = {arXiv},
arxivId = {arXiv:1011.1669v3},
author = {Woods, Stephen C. and Lotter, E C and McKay, L D and Porte, Daniel},
doi = {10.1038/282503a0},
eprint = {arXiv:1011.1669v3},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Woods et al. - 1979 - Chronic intracerebroventricular infusion of insulin reduces food intake and body weight of baboons.pdf:pdf},
isbn = {0028-0836 (Print)$\backslash$r0028-0836 (Linking)},
issn = {0028-0836},
journal = {Nature},
keywords = {insulin},
mendeley-tags = {insulin},
number = {5738},
pages = {503--505},
pmid = {116135},
title = {{Chronic intracerebroventricular infusion of insulin reduces food intake and body weight of baboons.}},
volume = {282},
year = {1979}
}
@article{Burkhart2008,
abstract = {The retinoblastoma (RB) tumour suppressor gene is functionally inactivated in a broad range of paediatric and adult cancers, and a plethora of cellular functions and partners have been identified for the RB protein. Data from human tumours and studies from mouse models indicate that loss of RB function contributes to both cancer initiation and progression. However, we still do not know the identity of the cell types in which RB normally prevents cancer initiation in vivo, and the specific functions of RB that suppress distinct aspects of the tumorigenic process are poorly understood.},
author = {Burkhart, Deborah L and Sage, Julien},
doi = {10.1038/nrc2399},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Burkhart, Sage - 2008 - Cellular mechanisms of tumour suppression by the retinoblastoma gene.pdf:pdf},
isbn = {1474-1768 (Electronic) 1474-175X (Linking)},
issn = {1474-175X},
journal = {Nat. Rev. Cancer},
keywords = {cancer},
mendeley-tags = {cancer},
number = {9},
pages = {671--682},
pmid = {18650841},
title = {{Cellular mechanisms of tumour suppression by the retinoblastoma gene.}},
volume = {8},
year = {2008}
}
@article{Ofei2005,
abstract = {Obesity is a common and preventable disease of clinical and public health importance. It is often a major risk factor for the development of several non-communicable diseases, significant disability and premature death. There is presently a global epidemic of obesity in all age groups and in both developed and developing countries. The increasing prevalence of obesity places a large burden on health care use and costs. Weight loss is associated with significant health and economic benefits. Effective weight loss strategies include dietary therapy, physical activity and lifestyle modification. Drug therapy is reserved for obese or overweight patients who have concomitant obesity-related risk factors or diseases. Population-wide prevention programmes have a greater potential of stemming the obesity epidemic and being more cost-effective than clinic-based weight-loss programmes. Ghana is going through an economic and nutrition transition and experiencing an increase in the prevalence of obesity and obesity-related illnesses, especially among women and urban dwellers. A national taskforce to address this epidemic and to draw up a national policy on related non-communicable diseases is urgently needed.},
author = {Ofei, F},
doi = {10.1182/blood-2005-07-2977},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Ofei - 2005 - Obesity - a preventable disease.pdf:pdf},
isbn = {0016-9560 (Print)$\backslash$r0016-9560 (Linking)},
issn = {0016-9560},
journal = {Ghana Med. J.},
keywords = {ab-,around the waist and,cardiovascular disease,hypertension,mellitus,non-communicable disease,obesity,overweight,the body - either,trunk,type 2 diabetes},
mendeley-tags = {obesity},
number = {3},
pages = {98--101},
pmid = {17299552},
title = {{Obesity - a preventable disease.}},
volume = {39},
year = {2005}
}
@article{Pulgaron2014,
author = {Pulgar{\'{o}}n, Elizabeth R.},
doi = {10.1016/j.clinthera.2012.12.014.Childhood},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Pulgar{\'{o}}n - 2014 - Childhood Obesity A Review of Increased Risk for Physical and Psychological Co-morbidities.pdf:pdf},
isbn = {3052430807},
journal = {Clin. Ther.},
keywords = {2013 excerpta medica,all correspondence concerning this,all rights reserved,article should be addressed,childhood obesity,department of pediatrics,division of,inc,medical co-morbidities,obesity,phd,psychological co-morbidities,pulgaron,to elizabeth r},
mendeley-tags = {obesity},
pages = {1--21},
title = {{Childhood Obesity: A Review of Increased Risk for Physical and Psychological Co-morbidities}},
volume = {35},
year = {2014}
}
@article{Bild2006,
abstract = {The development of an oncogenic state is a complex process involving the accumulation of multiple independent mutations that lead to deregulation of cell signalling pathways central to the control of cell growth and cell fate. The ability to define cancer subtypes, recurrence of disease and response to specific therapies using DNA microarray-based gene expression signatures has been demonstrated in multiple studies. Various studies have also demonstrated the potential for using gene expression profiles for the analysis of oncogenic pathways. Here we show that gene expression signatures can be identified that reflect the activation status of several oncogenic pathways. When evaluated in several large collections of human cancers, these gene expression signatures identify patterns of pathway deregulation in tumours and clinically relevant associations with disease outcomes. Combining signature-based predictions across several pathways identifies coordinated patterns of pathway deregulation that distinguish between specific cancers and tumour subtypes. Clustering tumours based on pathway signatures further defines prognosis in respective patient subsets, demonstrating that patterns of oncogenic pathway deregulation underlie the development of the oncogenic phenotype and reflect the biology and outcome of specific cancers. Predictions of pathway deregulation in cancer cell lines are also shown to predict the sensitivity to therapeutic agents that target components of the pathway. Linking pathway deregulation with sensitivity to therapeutics that target components of the pathway provides an opportunity to make use of these oncogenic pathway signatures to guide the use of targeted therapeutics.},
author = {Bild, Andrea H and Yao, Guang and Chang, Jeffrey T and Wang, Quanli and Potti, Anil and Chasse, Dawn and Joshi, Mary-Beth and Harpole, David and Lancaster, Johnathan M and Berchuck, Andrew and Olson, John a and Marks, Jeffrey R and Dressman, Holly K and West, Mike and Nevins, Joseph R},
doi = {10.1038/nature04296},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Bild et al.{\_}2006{\_}Oncogenic pathway signatures in human cancers as a guide to targeted therapies.pdf:pdf},
isbn = {1476-4687 (Electronic)},
issn = {0028-0836},
journal = {Nature},
number = {7074},
pages = {353--357},
pmid = {16273092},
title = {{Oncogenic pathway signatures in human cancers as a guide to targeted therapies.}},
volume = {439},
year = {2006}
}
@article{Jones1997,
abstract = {Black women with breast cancer are less likely than white women to be diagnosed while their disease is still at a localized stage. Racial differences in the prevalence of obesity in the United States have also been documented. This study was undertaken to determine the extent to which the observed racial difference in stage at diagnosis of breast cancer could be explained by racial differences in obesity, specifically severe obesity. This was a population-based, retrospective study of 145 black women and 177 white women in Connecticut who were diagnosed with breast cancer between January 1987 and March 1989. Severe obesity was associated with both race and stage at diagnosis: Black women were significantly more likely than white women to be severely obese (26{\%} vs. 7{\%}, respectively), and severe obesity was significantly associated with diagnosis at TNM stage II or greater (multivariate-adjusted odds ratio = 3.10, 95{\%} confidence interval (CI) 1.28-7.52). Adjustment for severe obesity in a logistic regression model reduced the risk of later stage at diagnosis in blacks relative to whites by 33{\%}, from an odds ratio of 1.98 (95{\%} CI 1.22-3.19) to one of 1.66 (95{\%} CI 1.01-2.73). The higher prevalence of severe obesity among black women may play an important role in explaining their relative disadvantage in stage at diagnosis of breast cancer.},
author = {Jones, B A and Kasi, S V and Curnen, M G and Owens, P H and Dubrow, R},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Jones et al.{\_}1997{\_}Severe obesity as an explanatory factor for the blackwhite difference in stage at diagnosis of breast cancer.pdf:pdf},
isbn = {0002-9262 (Print)},
issn = {0002-9262},
journal = {Am. J. Epidemiol.},
number = {5},
pages = {394--404},
pmid = {9290499},
title = {{Severe obesity as an explanatory factor for the black/white difference in stage at diagnosis of breast cancer.}},
volume = {146},
year = {1997}
}
@article{Ritchie2015,
author = {Ritchie, Matthew E and Phipson, Belinda and Wu, Di and Hu, Yifang and Law, Charity W and Shi, Wei and Smyth, Gordon K},
doi = {10.1093/nar/gkv007},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Ritchie et al. - 2015 - limma powers differential expression analyses for RNA-sequencing and microarray studies.pdf:pdf},
number = {7},
pages = {1--13},
title = {{limma powers differential expression analyses for RNA-sequencing and microarray studies}},
volume = {43},
year = {2015}
}
@article{Levine1997,
abstract = {The p53 gene and its protein product have become the center of intensive study ever since it became clear that slightly more than 50{\%} of human cancers contain mutations in this gene. An extensive database catalogs these mutations in more than 50 different cell and tissue types, although some types of cancers never appear to select for p53 mutations. The nature of these genetic changes in cancer cells is most commonly a missense mutation in one allele, producing a faulty protein that is then observed at high concentrations in these cells, followed by a reduction to homozygosity. More rarely, deletions or chain-termination mutations in the p53 gene indicate that the null phenotype predisposes to cancer, as has been observed in mice with a homozygous p53 null mutation. There have been some suggestions that the missense mutant producing a faulty p53 protein could contribute a "gain of function" phenotype, but this remains to be substantiated by additional experimentation.},
author = {Levine, Arnold J.},
doi = {10.1016/S0092-8674(00)81871-1},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Levine - 1997 - P53, the Cellular Gatekeeper for Growth and Division.pdf:pdf},
isbn = {0092-8674},
issn = {00928674},
journal = {Cell},
keywords = {cancer},
mendeley-tags = {cancer},
number = {3},
pages = {323--331},
pmid = {9039259},
title = {{P53, the Cellular Gatekeeper for Growth and Division}},
volume = {88},
year = {1997}
}
@article{Kelesidis2006,
author = {Kelesidis, I and Kelesidis, T and Mantzoros, C S},
doi = {10.1038/sj.bjc.6603051},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Kelesidis, Kelesidis, Mantzoros - 2006 - Adiponectin and cancer a systematic review.pdf:pdf},
journal = {Br. J. Cancer},
keywords = {2001,adipocytokines,adiponectin,also increased with,but their mortality is,cancer,developing cancer,environmental factors,especially when the bmi,increasing bmi,insulin resistance,is 4 40 kg,m {\`{a}} 2,more,obese subjects have not,obesity,only increased risk of,wolk et al},
mendeley-tags = {adiponectin,cancer,environmental factors},
pages = {1221--1225},
title = {{Adiponectin and cancer : a systematic review}},
volume = {94},
year = {2006}
}
@article{Roberts2010,
abstract = {Body mass index, as an approximation of body adiposity, is associated with increased risk of several common and less common malignancies in a sex- and site-specific manner. These findings implicate sex- and cancer site-specific biological mechanisms underpinning these associations, and it is unlikely that there is a "one system fits all" mechanism. Three main candidate systems have been proposed-insulin and the insulin-like growth factor-I axis, sex steroids, and adipokines-but there are shortfalls to these hypotheses. In this review, three novel candidate mechanisms are proposed: obesity-induced hypoxia, shared genetic susceptibility, and migrating adipose stromal cells. While public health policies aimed at curbing the underlying causes of the obesity epidemic are being implemented, there is a parallel need to better understand the biological processes linking obesity and cancer as a prerequisite to the development of new approaches to prevention and treatment.},
author = {Roberts, Darren L and Dive, Caroline and Renehan, Andrew G},
doi = {10.1146/annurev.med.080708.082713},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Roberts, Dive, Renehan - 2010 - Biological mechanisms linking obesity and cancer risk New perspectives.pdf:pdf},
isbn = {1545-326X (Electronic)$\backslash$r0066-4219 (Linking)},
issn = {0066-4219},
journal = {Annu. Rev. Med.},
keywords = {adipokines,genome-wide association,hypoxia,insulin resistance,insulin-like growth factors,obesity and cancer,sex steroids},
mendeley-tags = {obesity and cancer},
pages = {301--316},
pmid = {19824817},
title = {{Biological mechanisms linking obesity and cancer risk: New perspectives.}},
volume = {61},
year = {2010}
}
@article{Lee2008,
abstract = {Objective: To determine which simple index of overweight and obesity is the best discriminator of cardiovascular risk factors. Study Design and Setting: This is a meta-analysis of published literature. MEDLINE was searched. Studies that used receiver-operating characteristics (ROC) curve analysis and published area under the ROC curves (AUC) for overweight and obesity indices with hypertension, type-2 diabetes, and/or dyslipidemia were included. The AUC for each of the four indices, with each risk factor, was pooled using a random-effects model; male and female data were analyzed separately. Results: Ten studies met the inclusion criteria. Body mass index (BMI) was the poorest discriminator for cardiovascular risk factors. Waist-to-height ratio (WHtR) was the best discriminator for hypertension, diabetes, and dyslipidemia in both sexes; its pooled AUC (95{\%} confidence intervals) ranged from 0.67 (0.64, 0.69) to 0.73 (0.70, 0.75) and from 0.68 (0.63, 0.72) to 0.76 (0.70, 0.81) in males and females, respectively. Conclusion: Statistical evidence supports the superiority of measures of centralized obesity, especially WHtR, over BMI, for detecting cardiovascular risk factors in both men and women. ?? 2008 Elsevier Inc. All rights reserved.},
author = {Lee, Crystal Man Ying and Huxley, Rachel R. and Wildman, Rachel P. and Woodward, Mark},
doi = {10.1016/j.jclinepi.2007.08.012},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Lee et al. - 2008 - Indices of abdominal obesity are better discriminators of cardiovascular risk factors than BMI a meta-analysis.pdf:pdf},
isbn = {0895-4356},
issn = {08954356},
journal = {J. Clin. Epidemiol.},
keywords = {Body mass index,Cardiovascular risk factors,Meta-analysis,Obesity,ROC curve,Waist-to-height ratio,obesity},
mendeley-tags = {obesity},
number = {7},
pages = {646--653},
pmid = {18359190},
title = {{Indices of abdominal obesity are better discriminators of cardiovascular risk factors than BMI: a meta-analysis}},
volume = {61},
year = {2008}
}
@article{Jirtle2011,
abstract = {The Keystone symposium on 'Environmental Epigenomics and Disease Susceptibility' was held in late March 2011 at the Grove Park Inn Resort in Asheville, North Carolina, USA. The meeting helped to define the developing field of 'environmental epigenetics' and the research presented established its role in disease aetiology and susceptibility.},
archivePrefix = {arXiv},
arxivId = {GGPU9I},
author = {Jirtle, Randy L. and Skinner, Michael K},
doi = {10.1038/embor.2011.125},
eprint = {GGPU9I},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Jirtle, Skinner - 2011 - Environmental epigenomics and disease susceptibility.pdf:pdf},
isbn = {1471-0056 (Print)},
issn = {1750-1911},
journal = {EMBO Rep.},
keywords = {cancer,environmental factors},
mendeley-tags = {cancer,environmental factors},
number = {7},
pages = {620--622},
pmid = {21681201},
title = {{Environmental epigenomics and disease susceptibility.}},
volume = {12},
year = {2011}
}
@article{Law2014,
abstract = {New normal linear modeling strategies are presented for analyzing read counts from RNA-seq experiments. The voom method estimates the mean-variance relationship of the log-counts, generates a precision weight for each observation and enters these into the limma empirical Bayes analysis pipeline. This opens access for RNA-seq analysts to a large body of methodology developed for microarrays. Simulation studies show that voom performs as well or better than count-based RNA-seq methods even when the data are generated according to the assumptions of the earlier methods. Two case studies illustrate the use of linear modeling and gene set testing methods.},
author = {Law, Charity W. and Chen, Yunshun and Shi, Wei and Smyth, Gordon K.},
doi = {10.1186/gb-2014-15-2-r29},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Law et al. - 2014 - voom precision weights unlock linear model analysis tools for RNA-seq read counts.pdf:pdf},
isbn = {1465-6906},
issn = {1474-760X},
journal = {Genome Biol.},
pages = {R29},
pmid = {24485249},
title = {{voom: precision weights unlock linear model analysis tools for RNA-seq read counts}},
volume = {15},
year = {2014}
}
@article{Casellas2016,
abstract = {As B cells engage in the immune response, they express activation-induced cytidine deaminase (AID) to initiate the hypermutation and recombination of immunoglobulin genes, which are crucial processes for the efficient recognition and disposal of pathogens. However, AID must be tightly controlled in B cells to minimize off-target mutations, which can drive chromosomal translocations and the development of B cell malignancies, such as lymphomas. Recent genomic and biochemical analyses have begun to unravel the mechanisms of how AID-mediated deamination is targeted outside immunoglobulin genes. Here, we discuss the transcriptional and topological features that are emerging as key drivers of AID promiscuous activity.},
author = {Casellas, Rafael and Basu, Uttiya and Yewdell, William T. and Chaudhuri, Jayanta and Robbiani, Davide F. and {Di Noia}, Javier M.},
doi = {10.1038/nri.2016.2},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Casellas et al. - 2016 - Mutations, kataegis and translocations in B cells understanding AID promiscuous activity.pdf:pdf},
isbn = {1474-1733},
issn = {1474-1741},
journal = {Nat. Rev. Immunol.},
keywords = {cancer,kataegis},
mendeley-tags = {cancer,kataegis},
number = {3},
pages = {164--176},
pmid = {26898111},
publisher = {Nature Publishing Group},
title = {{Mutations, kataegis and translocations in B cells: understanding AID promiscuous activity.}},
volume = {16},
year = {2016}
}
@article{Kristensen1998,
abstract = {The mammalian hypothalamus strongly influences ingestive behaviour through several different signalling molecules and receptor systems. Here we show that CART (cocaine- and amphetamine-regulated transcript), a brain-located peptide, is a satiety factor and is closely associated with the actions of two important regulators of food intake, leptin and neuropeptide Y. Food-deprived animals show a pronounced decrease in expression of CART messenger RNA in the arcuate nucleus. In animal models of obesity with disrupted leptin signalling, CART mRNA is almost absent from the arcuate nucleus. Peripheral administration of leptin to obese mice stimulates CART mRNA expression. When injected intracerebroventricularly into rats, recombinant CART peptide inhibits both normal and starvation-induced feeding, and completely blocks the feeding response induced by neuropeptide Y. An antiserum against CART increases feeding in normal rats, indicating that CART may be an endogenous inhibitor of food intake in normal animals.},
author = {Kristensen, P and Judge, M E and Thim, L and Ribel, U and Christjansen, K N and Wulff, B S and Clausen, J T and Jensen, P B and Madsen, O D and Vrang, N and Larsen, P J and Hastrup, S},
doi = {10.1038/29993},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Kristensen et al. - 1998 - Hypothalamic CART is a new anorectic peptide regulated by leptin.pdf:pdf},
isbn = {0028-0836 (Print)},
issn = {0028-0836},
journal = {Nature},
number = {6680},
pages = {72--76},
pmid = {9590691},
title = {{Hypothalamic CART is a new anorectic peptide regulated by leptin.}},
volume = {393},
year = {1998}
}
@article{Goeman2007,
abstract = {Motivation: Many statistical tests have been proposed in recent years for analyzing gene expression data in terms of gene sets, usually from Gene Ontology. These methods are based on widely different methodological assumptions. Some approaches test differential expression of each gene set against differential expression of the rest of the genes, whereas others test each gene set on its own. Also, some methods are based on a model in which the genes are the sampling units, whereas others treat the subjects as the sampling units. This article aims to clarify the assumptions behind different approaches and to indicate a preferential methodology of gene set testing.$\backslash$nResults: We identify some crucial assumptions which are needed by the majority of methods. P-values derived from methods that use a model which takes the genes as the sampling unit are easily misinterpreted, as they are based on a statistical model that does not resemble the biological experiment actually performed. Furthermore, because these models are based on a crucial and unrealistic independence assumption between genes, the P-values derived from such methods can be wildly anti-conservative, as a simulation experiment shows. We also argue that methods that competitively test each gene set against the rest of the genes create an unnecessary rift between single gene testing and gene set testing.$\backslash$nContact: j.j.goeman@lumc.nl},
author = {Goeman, Jelle J. and B{\"{u}}hlmann, Peter},
doi = {10.1093/bioinformatics/btm051},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Goeman, B{\"{u}}hlmann - 2007 - Analyzing gene expression data in terms of gene sets Methodological issues.pdf:pdf},
isbn = {1367-4811 (Electronic)$\backslash$r1367-4803 (Linking)},
issn = {13674803},
journal = {Bioinformatics},
number = {8},
pages = {980--987},
pmid = {17303618},
title = {{Analyzing gene expression data in terms of gene sets: Methodological issues}},
volume = {23},
year = {2007}
}
@article{Adams1998,
abstract = {Bcl-2 and related cytoplasmic proteins are key regulators of apoptosis, the cell suicide program critical for development, tissue homeostasis, and protection against pathogens. Those most similar to Bcl-2 promote cell survival by inhibiting adapters needed for activation of the proteases (caspases) that dismantle the cell. More distant relatives instead promote apoptosis, apparently through mechanisms that include displacing the adapters from the pro-survival proteins. Thus, for many but not all apoptotic signals, the balance between these competing activities determines cell fate. Bcl-2 family members are essential for maintenance of major organ systems, and mutations affecting them are implicated in cancer.},
author = {Adams, J M and Cory, S},
doi = {10.1126/science.281.5381.1322},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Adams, Cory - 1998 - The Bcl-2 protein family arbiters of cell survival.pdf:pdf},
isbn = {0036-8075},
issn = {0036-8075},
journal = {Science (80-. ).},
keywords = {apoptosis,bcl2},
mendeley-tags = {apoptosis,bcl2},
number = {5381},
pages = {1322--1326},
pmid = {9735050},
title = {{The Bcl-2 protein family: arbiters of cell survival.}},
volume = {281},
year = {1998}
}
@article{Ames1995,
author = {Ames, Bruce N and Swirsky, Lois and Willettt, Walter C},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Ames, Swirsky, Willettt - 1995 - The causes and prevention of cancer.pdf:pdf},
journal = {Proc. Natl. Acad. Sci. USA},
keywords = {cancer,environmental factors},
mendeley-tags = {cancer,environmental factors},
pages = {5258--5265},
title = {{The causes and prevention of cancer}},
volume = {92},
year = {1995}
}
@article{Montague1997,
abstract = {The extreme obesity of the obese (ob/ob) mouse is attributable to mutations in the gene encoding leptin, an adipocyte-specific secreted protein which has profound effects on appetite and energy expenditure. We know of no equivalent evidence regarding leptin's role in the control of fat mass in humans. We have examined two severely obese children who are members of the same highly consanguineous pedigree. Their serum leptin levels were very low despite their markedly elevated fat mass and, in both, a homozygous frame-shift mutation involving the deletion of a single guanine nucleotide in codon 133 of the gene for leptin was found. The severe obesity found in these congenitally leptin-deficient subjects provides the first genetic evidence that leptin is an important regulator of energy balance in humans.},
author = {Montague, C T and Farooqi, I S and Whitehead, J P and Soos, M a and Rau, H and Wareham, N J and Sewter, C P and Digby, J E and Mohammed, S N and Hurst, J a and Cheetham, C H and Earley, a R and Barnett, a H and Prins, J B and O'Rahilly, S},
doi = {10.1038/43185},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Montague et al. - 1997 - Congenital leptin deficiency is associated with severe early-onset obesity in humans.pdf:pdf},
isbn = {0028-0836 (Print)},
issn = {0028-0836},
journal = {Nature},
keywords = {obesity},
mendeley-tags = {obesity},
number = {6636},
pages = {903--908},
pmid = {9202122},
title = {{Congenital leptin deficiency is associated with severe early-onset obesity in humans.}},
volume = {387},
year = {1997}
}
@article{Haupt1997,
abstract = {The p53 tumour-suppressor protein exerts antiproliferative effects, including growth arrest and apoptosis, in response to various types of stress. The activity of p53 is abrogated by mutations that occur frequently in tumours, as well as by several viral and cellular proteins. The Mdm2 oncoprotein is a potent inhibitor of p53. Mdm2 binds the transcriptional activation domain of p53 and blocks its ability to regulate target genes and to exert antiproliferative effects. On the other hand, p53 activates the expression of the mdm2 gene in an autoregulatory feedback loop. The interval between p53 activation and consequent Mdm2 accumulation defines a time window during which p53 exerts its effects. We now report that Mdm2 also promotes the rapid degradation of p53 under conditions in which p53 is otherwise stabilized. This effect of Mdm2 requires binding of p53; moreover, a small domain of p53, encompassing the Mdm2-binding site, confers Mdm2-dependent detstabilization upon heterologous proteins. Raised amounts of Mdm2 strongly repress mutant p53 accumulation in tumour-derived cells. During recovery from DNA damage, maximal Mdm2 induction coincides with rapid p53 loss. We propose that the Mdm2-promoted degradation of p53 provides a new mechanism to ensure effective termination of the p53 signal.},
author = {Haupt, Y and Maya, R and Kazaz, A and Oren, M},
doi = {10.1038/387296a0},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Haupt et al. - 1997 - Mdm2 promotes the rapid degradation of p53.pdf:pdf},
isbn = {0028-0836 (Print)},
issn = {0028-0836},
journal = {Nature},
keywords = {Animals,Cultured,Down-Regulation,Down-Regulation: radiation effects,HeLa Cells,Humans,Messenger,Messenger: metabolism,Mice,Nuclear Proteins,Protein Binding,Proto-Oncogene Proteins,Proto-Oncogene Proteins c-mdm2,Proto-Oncogene Proteins: genetics,Proto-Oncogene Proteins: metabolism,RNA,Recombinant Fusion Proteins,Recombinant Fusion Proteins: genetics,Recombinant Fusion Proteins: metabolism,Transfection,Tumor Cells,Tumor Suppressor Protein p53,Tumor Suppressor Protein p53: antagonists {\&} inhibi,Tumor Suppressor Protein p53: genetics,Tumor Suppressor Protein p53: metabolism,mdm2,p53},
mendeley-tags = {mdm2,p53},
number = {6630},
pages = {296--299},
pmid = {9153395},
title = {{Mdm2 promotes the rapid degradation of p53.}},
volume = {387},
year = {1997}
}
@article{Irizarry2003,
abstract = {SUMMARY In this paper we report exploratory analyses of high-density oligonucleotide array data from the Affymetrix GeneChip R system with the objective of improving upon currently used measures of gene expression. Our analyses make use of three data sets: a small experimental study consisting of five MGU74A mouse GeneChip R arrays, part of the data from an extensive spike-in study conducted by Gene Logic and Wyeth's Genetics Institute involving 95 HG-U95A human GeneChip R arrays; and part of a dilution study conducted by Gene Logic involving 75 HG-U95A GeneChip R arrays. We display some familiar features of the perfect match and mismatch probe (P M and M M) values of these data, and examine the variance–mean relationship with probe-level data from probes believed to be defective, and so delivering noise only. We explain why we need to normalize the arrays to one another using probe level intensities. We then examine the behavior of the P M and M M using spike-in data and assess three commonly used summary measures: Affymetrix's (i) average difference (AvDiff) and (ii) MAS 5.0 signal, and (iii) the Li and Wong multiplicative model-based expression index (MBEI). The exploratory data analyses of the probe level data motivate a new summary measure that is a robust multi-array average (RMA) of background-adjusted, normalized, and log-transformed P M values. We evaluate the four expression summary measures using the dilution study data, assessing their behavior in terms of bias, variance and (for MBEI and RMA) model fit. Finally, we evaluate the algorithms in terms of their ability to detect known levels of differential expression using the spike-in data. We conclude that there is no obvious downside to using RMA and attaching a standard error (SE) to this quantity using a linear model which removes probe-specific affinities.},
author = {Irizarry, Rafael A and Hobbs, Bridget and Collin, Francois and Beazer-Barclay, Yasmin D and Antonellis, Kristen J and Scherf, Uwe and Speed, Terence P},
doi = {10.1093/biostatistics/4.2.249},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Irizarry et al. - 2003 - Exploration, normalization, and summaries of high density oligonucleotide array probe level data.pdf:pdf},
isbn = {1465-4644 (Print) 1465-4644 (Linking)},
issn = {1465-4644},
journal = {Biostatistics},
number = {2},
pages = {249--264},
pmid = {12925520},
title = {{Exploration, normalization, and summaries of high density oligonucleotide array probe level data}},
volume = {4},
year = {2003}
}
@article{Engelman2009,
abstract = {There are ample genetic and laboratory studies that suggest the PI3K-Akt pathway is vital to the growth and survival of cancer cells. Inhibitors targeting this pathway are entering the clinic at a rapid pace. In this Review, the therapeutic potential of drugs targeting PI3K-Akt signalling for the treatment of cancer is discussed. I focus on the advantages and drawbacks of different treatment strategies for targeting this pathway, the cancers that might respond best to these therapies and the challenges and limitations that confront their clinical development.},
archivePrefix = {arXiv},
arxivId = {gr-qc/0208024},
author = {Engelman, J A},
doi = {10.1038/nrc2664},
eprint = {0208024},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Engelman - 2009 - Targeting PI3K signalling in cancer opportunities, challenges and limitations.pdf:pdf},
isbn = {1474-1768 (Electronic)$\backslash$r1474-175X (Linking)},
issn = {1474-1768},
journal = {Nat. Rev. Cancer},
keywords = {Antineoplastic Agents/pharmacology/ therapeutic us,Humans,Neoplasms/ drug therapy/ etiology/pathology,PI3K,Phosphatidylinositol 3-Kinases/ physiology,Protein Kinase Inhibitors/pharmacology/ therapeuti,Protein Kinases/physiology,Proto-Oncogene Proteins c-akt/ physiology,Signal Transduction/drug effects/ physiology,TOR Serine-Threonine Kinases,cancer},
mendeley-tags = {PI3K,cancer},
number = {8},
pages = {550--562},
pmid = {19629070},
primaryClass = {gr-qc},
publisher = {Nature Publishing Group},
title = {{Targeting PI3K signalling in cancer: opportunities, challenges and limitations}},
volume = {9},
year = {2009}
}
@misc{Keitt2012,
author = {Keitt, T},
title = {{colorRamps: Builds color tables}},
year = {2012}
}
@article{GO2000,
abstract = {Genomic sequencing has made it clear that a large fraction of the genes specifying the core biological functions are shared by all eukaryotes. Knowledge of the biological role of such shared proteins in one organism can often be transferred to other organisms. The goal of the Gene Ontology Consortium is to produce a dynamic, controlled vocabulary that can be applied to all eukaryotes even as knowledge of gene and protein roles in cells is accumulating and changing. To this end, three independent ontologies accessible on the World-Wide Web (http://www.geneontology.org) are being constructed: biological process, molecular function and cellular component.},
archivePrefix = {arXiv},
arxivId = {10614036},
author = {{Gene Ontology Consortium}},
doi = {10.1038/75556},
eprint = {10614036},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Gene Ontology Consortium - 2000 - Gene Ontology Tool for The Unification of Biology.pdf:pdf},
isbn = {1061-4036 (Print)$\backslash$r1061-4036 (Linking)},
issn = {1061-4036},
journal = {Nat. Genet.},
number = {1},
pages = {25--29},
pmid = {10802651},
title = {{Gene Ontology: Tool for The Unification of Biology}},
volume = {25},
year = {2000}
}
@article{Stratton2009,
abstract = {All cancers arise as a result of changes that have occurred in the DNA sequence of the genomes of cancer cells. Over the past quarter of a century much has been learnt about these mutations and the abnormal genes that operate in human cancers. We are now, however, moving into an era in which it will be possible to obtain the complete DNA sequence of large numbers of cancer genomes. These studies will provide us with a detailed and comprehensive perspective on how individual cancers have developed.},
author = {Stratton, Michael R and Campbell, Peter J and Futreal, P.Andrew Andrew},
doi = {10.1038/nature07943},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Stratton, Campbell, Futreal - 2009 - The cancer genome.pdf:pdf},
isbn = {1476-4687 (Electronic)$\backslash$r0028-0836 (Linking)},
issn = {0028-0836},
journal = {Nature},
keywords = {Genome,cancer,genes and mutations,review},
mendeley-tags = {cancer,genes and mutations,review},
number = {7239},
pages = {719--724},
pmid = {19360079},
publisher = {Nature Publishing Group},
title = {{The cancer genome}},
volume = {458},
year = {2009}
}
@article{Hernandez2013,
author = {Rodr{\'{i}}guez-Hern{\'{a}}ndez, Heriberto and Simental-Mend{\'{i}}a, Luis E and Rodr{\'{i}}guez-Ram{\'{i}}rez, Gabriela and Reyes-Romero, Miguel A},
doi = {10.1155/2013/678159},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Rodr{\'{i}}guez-Hern{\'{a}}ndez et al. - 2013 - Obesity and inflammation epidemiology, risk factors, and markers of inflammation.pdf:pdf},
isbn = {1687-8337 (Print)1687-8345 (Electronic)},
issn = {16878337},
journal = {Int. J. Endocrinol.},
keywords = {inflammation,obesity},
mendeley-tags = {inflammation,obesity},
pages = {1--11},
pmid = {23690772},
title = {{Obesity and inflammation: epidemiology, risk factors, and markers of inflammation}},
year = {2013}
}
@article{Elinav2013,
abstract = {Inflammation is a fundamental innate immune response to perturbed tissue homeostasis. Chronic inflammatory processes affect all stages of tumour development as well as therapy. In this Review, we outline the principal cellular and molecular pathways that coordinate the tumour-promoting and tumour-antagonizing effects of inflammation and we discuss the crosstalk between cancer development and inflammatory processes. In addition, we discuss the recently suggested role of commensal microorganisms in inflammation-induced cancer and we propose that understanding this microbial influence will be crucial for targeted therapy in modern cancer treatment.},
author = {Elinav, Eran and Nowarski, Roni and Thaiss, Christoph A and Hu, Bo and Jin, Chengcheng and Flavell, Richard A},
doi = {10.1038/nrc3611},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Elinav et al. - 2013 - Inflammation-induced cancer crosstalk between tumours, immune cells and microorganisms.pdf:pdf},
isbn = {1474-1768 (Electronic)$\backslash$r1474-175X (Linking)},
issn = {1474-1768},
journal = {Nat. Rev. Cancer},
keywords = {Animals,Carcinogenesis,Cell Proliferation,Cell Transformation,Gene Expression Regulation,Genome,Homeostasis,Humans,Immunity,Inflammation,Inflammation: complications,Inflammation: immunology,Inflammation: microbiology,Innate,Mice,Microbiota,Neoplasm Metastasis,Neoplasms,Neoplasms: etiology,Neoplasms: immunology,Neoplasms: microbiology,Neoplasms: pathology,Neoplastic,Neoplastic: immunology,Signal Transduction,cancer,inflammation},
mendeley-tags = {cancer,inflammation},
number = {11},
pages = {759--771},
pmid = {24154716},
title = {{Inflammation-induced cancer: crosstalk between tumours, immune cells and microorganisms.}},
volume = {13},
year = {2013}
}
@article{Gallagher2006,
abstract = {Solar ultraviolet radiation (UVR) has always been part of the environment of man. UVB is required for the conversion of 7-deoxycholesterol to vitamin D, which is critically important in the maintenance of healthy bones and research is making clear that it has other potential roles in maintenance of human health. Exposure to UVR, whether of solar or artificial origin, also carries potential risks to human health. UVR is a known carcinogen and excessive exposure-at least to solar radiation in sunlight-increases risk of cancer of the lip, basal cell, and squamous cell carcinoma of the skin and cutaneous melanoma, particularly in fair skin populations. There is also evidence that solar UVR increases risk of several diseases of the eye, including cortical cataract, some conjunctival neoplasms, and perhaps ocular melanoma. Solar UVR may also be involved in autoimmune and viral diseases although more research is needed in these areas. Artificial UVR from tanning beds, welding torches, and other sources, may contribute to the burden of disease from UVR. This brief review will assess the human evidence for adverse health effects from solar and artificial UVR and will attempt to assign a degree of certainty to the major disease-exposure relationships based on the weight of available scientific evidence. ?? 2006 Elsevier Ltd. All rights reserved.},
author = {Gallagher, Richard P. and Lee, Tim K.},
doi = {10.1016/j.pbiomolbio.2006.02.011},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Gallagher, Lee - 2006 - Adverse effects of ultraviolet radiation A brief review.pdf:pdf},
isbn = {0079-6107 (Print)$\backslash$n0079-6107 (Linking)},
issn = {00796107},
journal = {Prog. Biophys. Mol. Biol.},
keywords = {Cataract,Cutaneous melanoma,Ocular melanoma,Skin cancer,Sunlight,Ultraviolet radiation,cancer,environmental factors,uv},
mendeley-tags = {cancer,environmental factors,uv},
number = {1},
pages = {119--131},
pmid = {16580054},
title = {{Adverse effects of ultraviolet radiation: A brief review}},
volume = {92},
year = {2006}
}
@article{Claussnitzer2015a,
abstract = {BACKGROUND Genomewide association studies can be used to identify disease-relevant genomic regions, but interpretation of the data is challenging. The FTO region harbors the strongest genetic association with obesity, yet the mechanistic basis of this association remains elusive. METHODS We examined epigenomic data, allelic activity, motif conservation, regulator expression, and gene coexpression patterns, with the aim of dissecting the regulatory circuitry and mechanistic basis of the association between the FTO region and obesity. We validated our predictions with the use of directed perturbations in samples from patients and from mice and with endogenous CRISPR-Cas9 genome editing in samples from patients. RESULTS Our data indicate that the FTO allele associated with obesity represses mitochondrial thermogenesis in adipocyte precursor cells in a tissue-autonomous manner. The rs1421085 T-to-C single-nucleotide variant disrupts a conserved motif for the ARID5B repressor, which leads to derepression of a potent preadipocyte enhancer and a doubling of IRX3 and IRX5 expression during early adipocyte differentiation. This results in a cell-autonomous developmental shift from energy-dissipating beige (brite) adipocytes to energy-storing white adipocytes, with a reduction in mitochondrial thermogenesis by a factor of 5, as well as an increase in lipid storage. Inhibition of Irx3 in adipose tissue in mice reduced body weight and increased energy dissipation without a change in physical activity or appetite. Knockdown of IRX3 or IRX5 in primary adipocytes from participants with the risk allele restored thermogenesis, increasing it by a factor of 7, and overexpression of these genes had the opposite effect in adipocytes from nonrisk-allele carriers. Repair of the ARID5B motif by CRISPR-Cas9 editing of rs1421085 in primary adipocytes from a patient with the risk allele restored IRX3 and IRX5 repression, activated browning expression programs, and restored thermogenesis, increasing it by a factor of 7. CONCLUSIONS Our results point to a pathway for adipocyte thermogenesis regulation involving ARID5B, rs1421085, IRX3, and IRX5, which, when manipulated, had pronounced pro-obesity and anti-obesity effects. (Funded by the German Research Center for Environmental Health and others.).},
author = {Claussnitzer, Melina and Dankel, Simon N and Kim, Kyoung-Han and Quon, Gerald and Meuleman, Wouter and Haugen, Christine and Glunk, Viktoria and Sousa, Isabel S and Beaudry, Jacqueline L and Puviindran, Vijitha and Abdennur, Nezar A and Liu, Jannel and Svensson, Per-Arne and Hsu, Yi-Hsiang and Drucker, Daniel J and Mellgren, Gunnar and Hui, Chi-Chung and Hauner, Hans and Kellis, Manolis},
doi = {10.1056/NEJMoa1502214},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Claussnitzer et al. - 2015 - FTO Obesity Variant Circuitry and Adipocyte Browning in Humans.pdf:pdf},
isbn = {5383950753},
issn = {1533-4406},
journal = {N. Engl. J. Med.},
keywords = {FTO},
mendeley-tags = {FTO},
number = {10},
pages = {895--907},
pmid = {26287746},
title = {{FTO Obesity Variant Circuitry and Adipocyte Browning in Humans.}},
volume = {373},
year = {2015}
}
@article{Hawkes2007a,
abstract = {The pressure to regulate the marketing of high-energy, nutrient-poor foods to young people has been mounting in light of concern about rising worldwide levels of overweight and obesity. In 2004, the World Health Organization called on governments, industry, and civil society to act to reduce unhealthy marketing messages. Since then, important changes have taken place in the global regulatory environment regarding the marketing of food to young people. Industry has developed self-regulatory approaches, civil society has campaigned for statutory restrictions, and governments have dealt with a range of regulatory proposals. Still, there have been few new regulations that restrict food marketing to young people. Despite calls for evidence-based policy, new regulatory developments appear to have been driven less by evidence than by ethics.},
author = {Hawkes, Corinna},
doi = {10.2105/AJPH.2006.101162},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Hawkes - 2007 - Regulating and litigating in the public interest. Regulating food marketing to young people worldwide Trends and policy.pdf:pdf},
isbn = {0090-0036},
issn = {00900036},
journal = {Am. J. Public Health},
number = {11},
pages = {1962--1973},
pmid = {17901436},
title = {{Regulating and litigating in the public interest. Regulating food marketing to young people worldwide: Trends and policy drivers}},
volume = {97},
year = {2007}
}
@misc{gplots,
author = {Warnes, G.R. and Bolker, B. and Lodewijk, B. and Gentleman, R. and {Andy Liaw}, W.H. and Lumley, T. and Maechler, M. and Magnusson, A. and Steffen, M. and Schwartz, M. and Venables, B.},
title = {{gplots: Various R Programming Tools for Plotting Data}},
year = {2016}
}
@article{Weinstein2006,
abstract = {There has been considerable progress in the systemic treatment of cancer because of the rapid development and clinical application of molecular targeted agents. Although patients with a particular type and stage of cancer are often treated as a single group, more-specific therapy is being considered, as subsets of these patients who are more likely to benefit from treatment with particular agents are being identified. We previously introduced the concept of 'oncogene addiction' to explain how some cancers that contain multiple genetic, epigenetic, and chromosomal abnormalities are dependent on or 'addicted' to one or a few genes for both maintenance of the malignant phenotype and cell survival. Thus, reversal of only one or a few of these abnormalities can inhibit cancer cell growth and in some cases translate to improved survival rates. This review summarizes current experimental and clinical evidence for the concept of oncogene addiction and describes molecular mechanisms that may explain this phenomenon. In addition, we discuss how high-throughput screening methods, including gene-expression profiling and proteomics, and emerging methods for analyzing complex cellular networks can be used to identify the state of oncogene addiction, i.e. the 'Achilles' heel,' in specific cancers. Finally, we discuss the use of molecular targeted agents in combination with other anticancer agents as a strategy to optimize therapy and prevent disease recurrence.},
author = {Weinstein, I Bernard and Joe, Andrew K},
doi = {10.1038/ncponc0558},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Weinstein, Joe - 2006 - Mechanisms of disease Oncogene addiction--a rationale for molecular targeting in cancer therapy.pdf:pdf},
isbn = {1743-4254 (Print)$\backslash$r1743-4254 (Linking)},
issn = {1743-4254},
journal = {Nat. Clin. Pract. Oncol.},
keywords = {cancer,carcinogenesis,cell circuitry,combination therapy,molecular,oncogene addiction},
mendeley-tags = {cancer,oncogene addiction},
number = {8},
pages = {448--457},
pmid = {16894390},
title = {{Mechanisms of disease: Oncogene addiction--a rationale for molecular targeting in cancer therapy.}},
volume = {3},
year = {2006}
}
@article{Tomasetti2015a,
author = {Tomasetti, Cristian and Vogelstein, Bert},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Tomasetti, Vogelstein - 2015 - Cancer risk Role of environment.pdf:pdf},
journal = {Science (80-. ).},
keywords = {cancer,environmental factors},
mendeley-tags = {cancer,environmental factors},
number = {160},
pages = {730--731},
title = {{Cancer risk : Role of environment}},
volume = {347},
year = {2015}
}
@article{Kilpel??inen2011,
abstract = {BACKGROUND: The FTO gene harbors the strongest known susceptibility locus for obesity. While many individual studies have suggested that physical activity (PA) may attenuate the effect of FTO on obesity risk, other studies have not been able to confirm this interaction. To confirm or refute unambiguously whether PA attenuates the association of FTO with obesity risk, we meta-analyzed data from 45 studies of adults (n = 218,166) and nine studies of children and adolescents (n = 19,268).$\backslash$n$\backslash$nMETHODS AND FINDINGS: All studies identified to have data on the FTO rs9939609 variant (or any proxy [r(2){\textgreater}0.8]) and PA were invited to participate, regardless of ethnicity or age of the participants. PA was standardized by categorizing it into a dichotomous variable (physically inactive versus active) in each study. Overall, 25{\%} of adults and 13{\%} of children were categorized as inactive. Interaction analyses were performed within each study by including the FTO×PA interaction term in an additive model, adjusting for age and sex. Subsequently, random effects meta-analysis was used to pool the interaction terms. In adults, the minor (A-) allele of rs9939609 increased the odds of obesity by 1.23-fold/allele (95{\%} CI 1.20-1.26), but PA attenuated this effect (p(interaction) = 0.001). More specifically, the minor allele of rs9939609 increased the odds of obesity less in the physically active group (odds ratio = 1.22/allele, 95{\%} CI 1.19-1.25) than in the inactive group (odds ratio = 1.30/allele, 95{\%} CI 1.24-1.36). No such interaction was found in children and adolescents.$\backslash$n$\backslash$nCONCLUSIONS: The association of the FTO risk allele with the odds of obesity is attenuated by 27{\%} in physically active adults, highlighting the importance of PA in particular in those genetically predisposed to obesity.},
archivePrefix = {arXiv},
arxivId = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3206047{\&}tool=pmcentrez{\&}rendertype=abstract},
author = {Kilpelainen, Tuomas O. and Qi, Lu and Brage, Soren and Sharp, Stephen J. and Sonestedt, Emily and Demerath, Ellen and Ahmad, Tariq and Mora, Samia and Kaakinen, Marika and Sandholt, Camilla Helene and Holzapfel, Christina and Autenrieth, Christine S. and Hypp??nen, Elina and Cauchi, St??phane and He, Meian and Kutalik, Zoltan and Kumari, Meena and Stan????kov??, Alena and Meidtner, Karina and Balkau, Beverley and Tan, Jonathan T. and Mangino, Massimo and Timpson, Nicholas J. and Song, Yiqing and Zillikens, M. Carola and Jablonski, Kathleen A. and Garcia, Melissa E. and Johansson, Stefan and Bragg-Gresham, Jennifer L. and Wu, Ying and van Vliet-Ostaptchouk, Jana V. and Onland-Moret, N. Charlotte and Zimmermann, Esther and Rivera, Natalia V. and Tanaka, Toshiko and Stringham, Heather M. and Silbernagel, G??nther and Kanoni, Stavroula and Feitosa, Mary F. and Snitker, Soren and Ruiz, Jonatan R. and Metter, Jeffery and Larrad, Maria Teresa Martinez and Atalay, Mustafa and Hakanen, Maarit and Amin, Najaf and Cavalcanti-Proen??a, Christine and Gr??ntved, Anders and Hallmans, G??ran and Jansson, John Olov and Kuusisto, Johanna and K??h??nen, Mika and Lutsey, Pamela L. and Nolan, John J. and Palla, Luigi and Pedersen, Oluf and P??russe, Louis and Renstr??m, Frida and Scott, Robert A. and Shungin, Dmitry and Sovio, Ulla and Tammelin, Tuija H. and R??nnemaa, Tapani and Lakka, Timo A. and Uusitupa, Matti and Rios, Manuel Serrano and Ferrucci, Luigi and Bouchard, Claude and Meirhaeghe, Aline and Fu, Mao and Walker, Mark and Borecki, Ingrid B. and Dedoussis, George V. and Fritsche, Andreas and Ohlsson, Claes and Boehnke, Michael and Bandinelli, Stefania and van Duijn, Cornelia M. and Ebrahim, Shah and Lawlor, Debbie A. and Gudnason, Vilmundur and Harris, Tamara B. and S??rensen, Thorkild I A and Mohlke, Karen L. and Hofman, Albert and Uitterlinden, Andr?? G. and Tuomilehto, Jaakko and Lehtim??ki, Terho and Raitakari, Olli and Isomaa, Bo and Nj??lstad, P??l R. and Florez, Jose C. and Liu, Simin and Ness, Andy and Spector, Timothy D. and Tai, E. Shyong and Froguel, Philippe and Boeing, Heiner and Laakso, Markku and Marmot, Michael and Bergmann, Sven and Power, Chris and Khaw, Kay Tee and Chasman, Daniel and Ridker, Paul and Hansen, Torben and Monda, Keri L. and Illig, Thomas and J??rvelin, Marjo Riitta and Wareham, Nicholas J. and Hu, Frank B. and Groop, Leif C. and Orho-Melander, Marju and Ekelund, Ulf and Franks, Paul W. and Loos, Ruth J F},
doi = {10.1371/journal.pmed.1001116},
eprint = {/www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3206047{\&}tool=pmcentrez{\&}rendertype=abstract},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Kilpelainen et al. - 2011 - Physical activity attenuates the influence of FTO variants on obesity risk A meta-analysis of 218,166 adults.pdf:pdf},
isbn = {1549-1676 (Electronic)$\backslash$n1549-1277 (Linking)},
issn = {15491277},
journal = {PLoS Med.},
number = {11},
pages = {e1001116},
pmid = {22069379},
primaryClass = {http:},
title = {{Physical activity attenuates the influence of FTO variants on obesity risk: A meta-analysis of 218,166 adults and 19,268 children}},
volume = {8},
year = {2011}
}
@article{Ghilardi1996,
abstract = {Leptin and its receptor, obese receptor (OB-R), comprise an important signaling system for the regulation of body weight. Splice variants of OB-R mRNA encode proteins that differ in the length of their cytoplasmic domains. We cloned a long isoform of the wild-type leptin receptor that is preferentially expressed in the hypothalamus and show that it can activate signal transducers and activators of transcription (STAT)-3, STAT-5, and STAT-6. A point mutation within the OB-R gene of diabetic (db) mice generates a new splice donor site that dramatically reduces expression of this long isoform in homozygous db/db mice. In contrast, an OB-R protein with a shorter cytoplasmic domain is present in both db/db and wild-type mice. We show that this short isoform is unable to activate the STAT pathway. These data provide further evidence that the mutation in OB-R causes the db/db phenotype and identify three STAT proteins as potential mediators of the anti-obesity effects of leptin.},
author = {Ghilardi, N and Ziegler, S and Wiestner, A and Stoffel, R and Heim, M H and Skoda, R C},
doi = {10.1073/pnas.93.13.6231},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Ghilardi et al. - 1996 - Defective STAT signaling by the leptin receptor in diabetic mice.pdf:pdf},
isbn = {0027-8424},
issn = {0027-8424},
journal = {Proc. Natl. Acad. Sci. U. S. A.},
keywords = {Alternative Splicing,Animals,Base Sequence,Carrier Proteins,Carrier Proteins: genetics,Carrier Proteins: physiology,Cell Line,Cell Surface,DNA Primers,DNA-Binding Proteins,DNA-Binding Proteins: metabolism,Diabetes Mellitus,Exons,Experimental,Experimental: metabolism,Humans,Inbred C57BL,Introns,Leptin,Mice,Milk Proteins,Molecular Sequence Data,Receptors,STAT3 Transcription Factor,STAT5 Transcription Factor,STAT6 Transcription Factor,Signal Transduction,Signal Transduction: genetics,Trans-Activators,Trans-Activators: metabolism,leptin},
mendeley-tags = {leptin},
number = {13},
pages = {6231--6235},
pmid = {8692797},
title = {{Defective STAT signaling by the leptin receptor in diabetic mice.}},
volume = {93},
year = {1996}
}
@article{McLaren2007,
abstract = {The objective of this review was to update Sobal and Stunkard's exhaustive review of the literature on the relation between socioeconomic status (SES) and obesity (Psychol Bull 1989;105:260–75). Diverse research databases (including CINAHL, ERIC, MEDLINE, and Social Science Abstracts) were comprehensively searched during the years 1988–2004 inclusive, using “obesity,” “socioeconomic status,” and synonyms as search terms. A total of 333 published studies, representing 1,914 primarily cross-sectional associations, were included in the review. The overall pattern of results, for both men and women, was of an increasing proportion of positive associations and a decreasing proportion of negative associations as one moved from countries with high levels of socioeconomic development to countries with medium and low levels of development. Findings varied by SES indicator; for example, negative associations (lower SES associated with larger body size) for women in highly developed countries were most common with education and occupation, while positive associations for women in medium- and low-development countries were most common with income and material possessions. Patterns for women in higher- versus lower-development countries were generally less striking than those observed by Sobal and Stunkard; this finding is interpreted in light of trends related to globalization. Results underscore a view of obesity as a social phenomenon, for which appropriate action includes targeting both economic and sociocultural factors.},
author = {McLaren, Lindsay},
doi = {10.1093/epirev/mxm001},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/McLaren - 2007 - Socioeconomic status and obesity.pdf:pdf},
isbn = {9780199940684},
issn = {0193936X},
journal = {Epidemiol. Rev.},
keywords = {Developing countries,Obesity,Review [publication type],Sex,Social class,obesity},
mendeley-tags = {obesity},
pages = {29--48},
pmid = {17478442},
title = {{Socioeconomic status and obesity}},
volume = {29},
year = {2007}
}
@article{Dar2012,
abstract = {The complexity of cancer has led to recent interest in polypharmacological approaches for developing kinase-inhibitor drugs; however, optimal kinase-inhibition profiles remain difficult to predict. Using a Ret-kinase-driven Drosophila model of multiple endocrine neoplasia type 2 and kinome-wide drug profiling, here we identify that AD57 rescues oncogenic Ret-induced lethality, whereas related Ret inhibitors imparted reduced efficacy and enhanced toxicity. Drosophila genetics and compound profiling defined three pathways accounting for the mechanistic basis of efficacy and dose-limiting toxicity. Inhibition of Ret plus Raf, Src and S6K was required for optimal animal survival, whereas inhibition of the 'anti-target' Tor led to toxicity owing to release of negative feedback. Rational synthetic tailoring to eliminate Tor binding afforded AD80 and AD81, compounds featuring balanced pathway inhibition, improved efficacy and low toxicity in Drosophila and mammalian multiple endocrine neoplasia type 2 models. Combining kinase-focused chemistry, kinome-wide profiling and Drosophila genetics provides a powerful systems pharmacology approach towards developing compounds with a maximal therapeutic index.},
archivePrefix = {arXiv},
arxivId = {NIHMS150003},
author = {Dar, Arvin C and Das, Tirtha K and Shokat, Kevan M and Cagan, Ross L},
doi = {10.1038/nature11127},
eprint = {NIHMS150003},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Dar et al. - 2012 - Chemical genetic discovery of targets and anti-targets for cancer polypharmacology.pdf:pdf},
isbn = {1476-4687 (Electronic) 0028-0836 (Linking)},
issn = {1476-4687},
journal = {Nature},
keywords = {pathway crosstalk},
mendeley-tags = {pathway crosstalk},
number = {7401},
pages = {80--84},
pmid = {22678283},
publisher = {Nature Publishing Group},
title = {{Chemical genetic discovery of targets and anti-targets for cancer polypharmacology.}},
volume = {486},
year = {2012}
}
@article{Lee1996,
author = {Lee, Gwo-Hwa and Proenca, R. and Montez, J. M. and Carroll, K. M. and Darvishzadeh, J. G. and Lee, J. I. and Friedman, J M},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Lee et al. - 1996 - Abnormal splicing of the leptin receptor in diabetic mice.pdf:pdf},
journal = {Nature},
keywords = {leptin},
mendeley-tags = {leptin},
pages = {632--635},
title = {{Abnormal splicing of the leptin receptor in diabetic mice}},
volume = {379},
year = {1996}
}
@article{Dalton2003,
author = {Dalton, M. and Cameron, A.J. and Zimmet, P.Z. and Shaw, J.E. and Jolley, D. and Dunstan, D.W. and Welborn, T.A.},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Dalton et al. - 2003 - Waist circumference, waist–hip ratio and body mass indexand their correlation with cardiovascular disease risk.pdf:pdf},
journal = {J. Intern. Med.},
keywords = {body mass index,body size,hip ratio,obesity,waist,waist circumference},
pages = {555--563},
title = {{Waist circumference, waist–hip ratio and body mass indexand their correlation with cardiovascular disease risk factorsin Australian adults.}},
volume = {254},
year = {2003}
}
@article{Krude1998,
abstract = {Sequential cleavage of the precursor protein pre-pro-opiomelanocortin (POMC) generates the melanocortin peptides adrenocorticotrophin (ACTH), melanocyte-stimulating hormones (MSH) alpha, beta and gamma as well as the opioid-receptor ligand beta-endorphin. While a few cases of isolated ACTH deficiency have been reported (OMIM 201400), an inherited POMC defect has not been described so far. Recent studies in animal models elucidated a central role of alpha-MSH in the regulation of food intake by activation of the brain melanocortin-4-receptor (MC4-R; refs 3-5) and the linkage of human obesity to chromosome 2 in close proximity to the POMC locus, led to the proposal of an association of POMC with human obesity. The dual role of alpha-MSH in regulating food intake and influencing hair pigmentation predicts that the phenotype associated with a defect in POMC function would include obesity, alteration in pigmentation and ACTH deficiency. The observation of these symptoms in two probands prompted us to search for mutations within their POMC genes. Patient 1 was found to be a compound heterozygote for two mutations in exon 3 (G7013T, C7133delta) which interfere with appropriate synthesis of ACTH and alpha-MSH. Patient 2 was homozygous for a mutation in exon 2 (C3804A) which abolishes POMC translation. These findings represent the first examples of a genetic defect within the POMC gene and define a new monogenic endocrine disorder resulting in early-onset obesity, adrenal insufficiency and red hair pigmentation.},
author = {Krude, H and Biebermann, H and Luck, W and Horn, R and Brabant, G and Gr{\"{u}}ters, a},
doi = {10.1177/000992289903800416},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Krude et al. - 1998 - Severe early-onset obesity, adrenal insufficiency and red hair pigmentation caused by POMC mutations in humans.pdf:pdf},
isbn = {1061-4036 (Print)$\backslash$r1061-4036 (Linking)},
issn = {0009-9228},
journal = {Nat. Genet.},
keywords = {obesity},
mendeley-tags = {obesity},
number = {2},
pages = {155--157},
pmid = {9620771},
title = {{Severe early-onset obesity, adrenal insufficiency and red hair pigmentation caused by POMC mutations in humans.}},
volume = {19},
year = {1998}
}
@misc{Girke2016,
author = {Girke, T},
title = {{overLapper.R}},
year = {2016}
}
@article{Kalluri2009,
abstract = {he origins of the mesenchymal cells participating in tissue repair and pathological processes, notably tissue fibrosis, tumor invasiveness, and metastasis, are poorly understood. However, emerging evidence suggests that epithelial-mesenchymal transitions (EMTs) represent one important source of these cells. As we discuss here, processes similar to the EMTs associated with embryo implantation, embryogenesis, and organ development are appropriated and subverted by chronically inflamed tissues and neoplasias. The identification of the signaling pathways that lead to activation of EMT programs during these disease processes is providing new insights into the plasticity of cellular phenotypes and possible therapeutic interventions},
archivePrefix = {arXiv},
arxivId = {arXiv:cond-mat/0402594v3},
author = {Kalluri, Raghu and Weinberg, Robert a},
doi = {10.1172/JCI39104.1420},
eprint = {0402594v3},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Kalluri, Weinberg - 2009 - Review series The basics of epithelial-mesenchymal transition.pdf:pdf},
isbn = {1558-8238 (Electronic)$\backslash$r0021-9738 (Linking)},
issn = {0021-9738},
journal = {J. Clin. Invest.},
keywords = {EMT,cancer,metastasis},
mendeley-tags = {EMT,cancer,metastasis},
number = {6},
pages = {1420--1428},
pmid = {19487818},
primaryClass = {arXiv:cond-mat},
title = {{Review series The basics of epithelial-mesenchymal transition}},
volume = {119},
year = {2009}
}
@article{Nakazato2001,
abstract = {Ghrelin is an acylated peptide that stimulates the release of growth hormone from the pituitary. Ghrelin-producing neurons are located in the hypothalamus, whereas ghrelin receptors are expressed in various regions of the brain, which is indicative of central-and as yet undefined-physiological functions. Here we show that ghrelin is involved in the hypothalamic regulation of energy homeostasis. Intracerebroventricular injections of ghrelin strongly stimulated feeding in rats and increased body weight gain. Ghrelin also increased feeding in rats that are genetically deficient in growth hormone. Anti-ghrelin immunoglobulin G robustly suppressed feeding. After intracerebroventricular ghrelin administration, Fos protein, a marker of neuronal activation, was found in regions of primary importance in the regulation of feeding, including neuropeptide Y6 (NPY) neurons and agouti-related protein (AGRP) neurons. Antibodies and antagonists of NPY and AGRP abolished ghrelin-induced feeding. Ghrelin augmented NPY gene expression and blocked leptin-induced feeding reduction, implying that there is a competitive interaction between ghrelin and leptin in feeding regulation. We conclude that ghrelin is a physiological mediator of feeding, and probably has a function in growth regulation by stimulating feeding and release of growth hormone.},
author = {Nakazato, M and Murakami, N and Date, Y and Kojima, M and Matsuo, H and Kangawa, K and Matsukura, S},
doi = {10.1038/35051587},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Nakazato et al. - 2001 - A role for ghrelin in the central regulation of feeding.pdf:pdf},
isbn = {0028-0836 (Print)$\backslash$r0028-0836 (Linking)},
issn = {0028-0836},
journal = {Nature},
number = {6817},
pages = {194--198},
pmid = {11196643},
title = {{A role for ghrelin in the central regulation of feeding}},
volume = {409},
year = {2001}
}
@article{Wiseman2002,
abstract = {Breast cancer manifests itself in the mammary epithelium, yet there is a growing recognition that mammary stromal cells also play an important role in tumorigenesis. During its developmental cycle, the mammary gland displays many of the properties associated with breast cancer, and many of the stromal factors necessary for mammary development also promote or protect against breast cancer. Here we review our present knowledge of the specific factors and cell types that contribute to epithelial-stromal crosstalk during mammary development. To find cures for diseases like breast cancer that rely on epithelial-stromal crosstalk, we must understand how these different cell types communicate with each other.},
author = {Wiseman, Bryony S. and Werb, Zena},
doi = {10.1126/science.1067431.Stromal},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Wiseman, Werb - 2002 - Stromal Effects on Mammary Gland Development and Breast Cancer.pdf:pdf},
isbn = {0036-8075},
issn = {0036-8075, 1095-9203},
journal = {Science (80-. ).},
keywords = {cancer},
mendeley-tags = {cancer},
number = {5570},
pages = {1046--1049},
pmid = {12004111},
title = {{Stromal Effects on Mammary Gland Development and Breast Cancer}},
volume = {296},
year = {2002}
}
@article{Tartaglia1995,
abstract = {The ob gene product, leptin, is an important circulating signal for the regulation of body weight. To identify high affinity leptin-binding sites, we generated a series of leptin-alkaline phosphatase (AP) fusion proteins as well as [125I]leptin. After a binding survey of cell lines and tissues, we identified leptin-binding sites in the mouse choroid plexus. A cDNA expression library was prepared from mouse choroid plexus and screened with a leptin-AP fusion protein to identify a leptin receptor (OB-R). OB-R is a single membrane-spanning receptor most related to the gp130 signal-transducing component of the IL-6 receptor, the G-CSF receptor, and the LIF receptor. OB-R mRNA is expressed not only in choroid plexus, but also in several other tissues, including hypothalamus. Genetic mapping of the gene encoding OB-R shows that it is within the 5.1 cM interval of mouse chromosome 4 that contains the db locus. {\textcopyright} 1995.},
author = {Tartaglia, Louis A. and Dembski, Marlene and Weng, Xun and Deng, Nanhua and Culpepper, Janice and Devos, Rene and Richards, Grayson J. and Campfield, L. Arthur and Clark, Frederick T. and Deeds, Jim and Muir, Craig and Sanker, Sean and Moriarty, Ann and Moore, Karen J. and Smutko, John S. and Mays, Gail G. and Wool, Elizabeth A. and Monroe, Cheryl A. and Tepper, Robert I.},
doi = {10.1016/0092-8674(95)90151-5},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Tartaglia et al. - 1995 - Identification and expression cloning of a leptin receptor, OB-R.pdf:pdf},
isbn = {0092-8674 (Print)},
issn = {00928674},
journal = {Cell},
keywords = {obesity},
mendeley-tags = {obesity},
number = {7},
pages = {1263--1271},
pmid = {8548812},
title = {{Identification and expression cloning of a leptin receptor, OB-R}},
volume = {83},
year = {1995}
}
@article{Golub1970,
abstract = {The matrix U consists of n orthonormalized eigenvectors associated with the n largest eigenvalues of AA r, and the matrix V consists of the orthonormalized eigenvectors of AZ A. The diagonal elements of 27 are the non-negative square roots of the eigenvalues of ATA; they are ...},
author = {Golub, G. H. and Reinsch, C.},
doi = {10.1007/BF02163027},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Golub, Reinsch - 1970 - Singular value decomposition and least squares solutions.pdf:pdf},
isbn = {0029-599X},
issn = {0029599X},
journal = {Numer. Math.},
number = {5},
pages = {403--420},
title = {{Singular value decomposition and least squares solutions}},
volume = {14},
year = {1970}
}
@article{Niswender2003,
author = {Niswender, Kevin D and Morrison, Christopher D and Clegg, Deborah J and Olson, Ryan and Baskin, Denis G and Myers, Martin G and Seeley, Randy J and Schwartz, Michael W},
doi = {10.2337/diabetes.52.2.227},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Niswender et al. - 2003 - Insulin Activation of Phosphatidylinositol 3-Kinase in the Hypothalamic Arcuate Nucleus A Key Mediator of Insu.pdf:pdf},
journal = {Diabetes},
keywords = {obesity},
mendeley-tags = {obesity},
pages = {227--231},
title = {{Insulin Activation of Phosphatidylinositol 3-Kinase in the Hypothalamic Arcuate Nucleus: A Key Mediator of Insulin-Induced Anorexia}},
volume = {52},
year = {2003}
}
@article{Carmeliet2000,
author = {Carmeliet, Peter and Jain, Rakesh K},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Carmeliet, Jain - 2000 - Angiogenesis in cancer and other diseases.pdf:pdf},
journal = {Nature},
keywords = {angiogenesis,cancer},
mendeley-tags = {angiogenesis,cancer},
pages = {249--257},
title = {{Angiogenesis in cancer and other diseases}},
volume = {407},
year = {2000}
}
@article{Wilhelm2006,
abstract = {Since the molecular revolution of the 1980s, knowledge of the aetiology of cancer has increased considerably, which has led to the discovery and development of targeted therapies tailored to inhibit cancer-specific pathways. The introduction and refinement of rapid, high-throughput screening technologies over the past decade has greatly facilitated this targeted discovery and development process. Here, we describe the discovery and continuing development of sorafenib (previously known as BAY 43-9006), the first oral multikinase inhibitor that targets Raf and affects tumour signalling and the tumour vasculature. The discovery cycle of sorafenib (Nexavar; Bayer Pharmaceuticals) - from initial screening for a lead compound to FDA approval for the treatment of advanced renal cell carcinoma in December 2005 - was completed in just 11 years, with approval being received approximately 5 years after the initiation of the first Phase I trial.},
author = {Wilhelm, Scott and Carter, Christopher and Lynch, Mark and Lowinger, Timothy and Dumas, Jacques and Smith, Roger a and Schwartz, Brian and Simantov, Ronit and Kelley, Susan},
doi = {10.1038/nrd2130},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Wilhelm et al. - 2006 - Discovery and development of sorafenib a multikinase inhibitor for treating cancer.pdf:pdf},
isbn = {1474-1776 (Print)$\backslash$r1474-1776 (Linking)},
issn = {1474-1776},
journal = {Nat. Rev. Drug Discov.},
keywords = {cancer,sorafenib},
mendeley-tags = {cancer,sorafenib},
number = {10},
pages = {835--844},
pmid = {17016424},
title = {{Discovery and development of sorafenib: a multikinase inhibitor for treating cancer.}},
volume = {5},
year = {2006}
}
@article{Leibowitz2015,
author = {Leibowitz, Mitchell L. and Zhang, Cheng-Zhong and Pellman, David},
doi = {10.1146/annurev-genet-120213-092228},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Leibowitz, Zhang, Pellman - 2015 - Chromothripsis A New Mechanism for Rapid Karyotype Evolution.pdf:pdf},
issn = {0066-4197},
journal = {Annu. Rev. Genet.},
keywords = {cancer,chromosome bridge,chromothripsis,complex chromosomal rearrangement,genome evolution,micronuclei,nuclear envelope rupture,single-cell sequencing},
mendeley-tags = {cancer,chromothripsis},
number = {1},
pages = {183--211},
title = {{Chromothripsis: A New Mechanism for Rapid Karyotype Evolution}},
volume = {49},
year = {2015}
}
@article{Spanswick2000,
abstract = {Insulin and leptin receptors are present in hypothalamic regions that control energy homeostasis, and these hormones reduce food intake and body weight in lean, but not obese, Zucker rats. Here we demonstrate that insulin, like leptin, hyperpolarizes lean rat hypothalamic glucose-responsive (GR) neurons by opening KATP channels. These findings suggest hypothalamic K ATP channel function is crucial to physiological regulation of food intake and body weight.},
author = {Spanswick, D and Smith, M a and Mirshamsi, S and Routh, V H and Ashford, M L},
doi = {10.1038/77660},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Spanswick et al. - 2000 - Insulin activates ATP-sensitive K channels in hypothalamic neurons of lean, but not obese rats.pdf:pdf},
isbn = {1097-6256 (Print)$\backslash$r1097-6256 (Linking)},
issn = {1097-6256},
journal = {Nat. Neurosci.},
keywords = {insulin},
mendeley-tags = {insulin},
number = {8},
pages = {757--758},
pmid = {10903566},
title = {{Insulin activates ATP-sensitive K+ channels in hypothalamic neurons of lean, but not obese rats.}},
volume = {3},
year = {2000}
}
@article{Wu2012,
abstract = {Competitive gene set tests are commonly used in molecular pathway analysis to test for enrichment of a particular gene annotation category amongst the differential expression results from a microarray experiment. Existing gene set tests that rely on gene permutation are shown here to be extremely sensitive to inter-gene correlation. Several data sets are analyzed to show that inter-gene correlation is non-ignorable even for experiments on homogeneous cell populations using genetically identical model organisms. A new gene set test procedure (CAMERA) is proposed based on the idea of estimating the inter-gene correlation from the data, and using it to adjust the gene set test statistic. An efficient procedure is developed for estimating the inter-gene correlation and characterizing its precision. CAMERA is shown to control the type I error rate correctly regardless of inter-gene correlations, yet retains excellent power for detecting genuine differential expression. Analysis of breast cancer data shows that CAMERA recovers known relationships between tumor subtypes in very convincing terms. CAMERA can be used to analyze specified sets or as a pathway analysis tool using a database of molecular signatures.},
author = {Wu, Di and Smyth, Gordon K.},
doi = {10.1093/nar/gks461},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Wu, Smyth - 2012 - Camera A competitive gene set test accounting for inter-gene correlation.pdf:pdf},
isbn = {1362-4962 (Electronic) 0305-1048 (Linking)},
issn = {03051048},
journal = {Nucleic Acids Res.},
number = {17},
pages = {e133},
pmid = {22638577},
title = {{Camera: A competitive gene set test accounting for inter-gene correlation}},
volume = {40},
year = {2012}
}
@article{Hecht1999,
abstract = {The complexity of tobacco smoke leads to some confusion about the$\backslash$nmechanisms by which it causes lung cancer. Among the multiple components$\backslash$nof tobacco smoke, 20 carcinogens convincingly cause lung tumors in$\backslash$nlaboratory animals or humans and are, therefore, likely to be involved$\backslash$nin lung cancer induction. Of these, polycyclic aromatic hydrocarbons$\backslash$nand the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone$\backslash$nare likely to play major roles. This review focuses on carcinogens$\backslash$nin tobacco smoke as a means of simplifying and clarifying the relevant$\backslash$ninformation that provides a mechanistic framework linking nicotine$\backslash$naddiction with lung cancer through exposure to such compounds. Included$\backslash$nis a discussion of the mechanisms by which tobacco smoke carcinogens$\backslash$ninteract with DNA and cause genetic changes--mechanisms that are$\backslash$nreasonably well understood--and the less well defined relationship$\backslash$nbetween exposure to specific tobacco smoke carcinogens and mutations$\backslash$nin oncogenes and tumor suppressor genes. Molecular epidemiologic$\backslash$nstudies of gene-carcinogen interactions and lung cancer--an approach$\backslash$nthat has not yet reached its full potential--are also discussed,$\backslash$nas are inhalation studies of tobacco smoke in laboratory animals$\backslash$nand the potential role of free radicals and oxidative damage in tobacco-associated$\backslash$ncarcinogenesis. By focusing in this review on several important carcinogens$\backslash$nin tobacco smoke, the complexities in understanding tobacco-induced$\backslash$ncancer can be reduced, and new approaches for lung cancer prevention$\backslash$ncan be envisioned.},
author = {Hecht, S.S.},
doi = {10.1093/jnci/91.14.1194},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Hecht - 1999 - Tobacco smoke carcinogen and lung cancer.pdf:pdf},
isbn = {9781617379949},
issn = {0027-8874},
journal = {J. Natl. Cancer Inst.},
keywords = {environmental factors,lung cancer,tobacco},
mendeley-tags = {environmental factors,lung cancer,tobacco},
number = {14},
pages = {1194--1210},
pmid = {10413421},
title = {{Tobacco smoke carcinogen and lung cancer}},
volume = {91},
year = {1999}
}
@article{Newton2004,
abstract = {This year marks the 25-year anniversary of the discovery by Nishizuka and co-workers that diacylglycerol activates the ubiquitous signal transducer protein kinase C. This discovery placed the lipid second messenger-protein kinase C signaling pathway center stage alongside the cAMP-protein kinase A pathway, which was already established as a fundamental mechanism for transducing extracellular signals.},
author = {Hofseth, Lorne J. and Hussain, S. Perwez and Harris, Curtis. C.},
doi = {10.1016/j.tips.2004.02.010},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Hofseth, Hussain, Harris - 2004 - p53 25 years after its discovery.pdf:pdf},
isbn = {0165-6147 (Print)$\backslash$r0165-6147 (Linking)},
issn = {01656147},
journal = {Trends Pharmacol. Sci.},
keywords = {cancer,p53},
mendeley-tags = {cancer,p53},
number = {4},
pages = {177--181},
pmid = {15116719},
title = {p53: 25 years after its discovery},
volume = {25},
year = {2004}
}
@article{Shaffer1995,
author = {Shaffer, Juliet Popper},
doi = {10.1016/S1573-4412(84)02006-7},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Shaffer - 1995 - Multiple hypothesis testing.pdf:pdf},
isbn = {9780444861863},
issn = {15734412},
journal = {Annu. Rev. Psychol.},
pages = {561--584},
title = {{Multiple hypothesis testing}},
volume = {46},
year = {1995}
}
@article{WHO2000,
author = {{World Health Organisation}},
doi = {10.1016/S0140-6736(03)15268-3},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/World Health Organisation - 2000 - Obesity preventing and managing the global epidemic.pdf:pdf;:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/World Health Organisation - 2000 - Obesity preventing and managing the global epidemic(2).pdf:pdf;:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/World Health Organisation - 2000 - Obesity preventing and managing the global epidemic(3).pdf:pdf},
isbn = {9241208945},
issn = {0512-3054},
keywords = {obesity},
mendeley-tags = {obesity},
pages = {6--8},
pmid = {11234459},
title = {{Obesity : preventing and managing the global epidemic}},
volume = {894},
year = {2000}
}
@article{Gatza2011,
abstract = {INTRODUCTION: Breast cancer heterogeneity occurs as a consequence of the dysregulation of numerous oncogenic pathways as well as many non-genetic factors, including tumor microenvironmental stresses such as hypoxia, lactic acidosis, and glucose deprivation. Although the importance of these non-genetic factors is well recognized, it is not clear how to integrate these factors within the genetic framework of cancer as the next logical step in understanding tumor heterogeneity.$\backslash$n$\backslash$nMETHODS: We report here the development of a series of gene expression signatures to measure the influences of microenvironmental stresses. The pathway activities of hypoxia, lactic acidosis, acidosis and glucose deprivation were investigated in a collection of 1,143 breast tumors, which have been separated into 17 breast tumor subgroups defined by their distinct patterns of oncogenic pathways. A validation dataset comprised of 547 breast tumors was also used to confirm the major findings, and representative breast cancer cell lines were utilized to validate in silico results and mechanistic studies.$\backslash$n$\backslash$nRESULTS: Through the integrative pathway analysis of microenvironmental stresses and oncogenic events in breast tumors, we identified many known and novel correlations between these two sources of tumor heterogeneity. Focusing on differences between two human epidermal growth factor receptor 2 (HER2)-related subgroups, previously identified based on patterns of oncogenic pathway activity, we determined that these subgroups differ with regards to tumor microenvironmental signatures, including hypoxia. We further demonstrate that each of these subgroups have features consistent with basal and luminal breast tumors including patterns of oncogenic signaling pathways, expression of subtype specific genes, and cellular mechanisms that regulate the hypoxia response. Importantly, we also demonstrate that the correlated pattern of hypoxia-related gene expression and basal-associated gene expression are consistent across HER2-related tumors whether we analyze the tumors as a function of our pathway-based classification scheme, using the intrinsic gene list (ERBB2+), or based on HER2 IHC status. Our results demonstrate a cell lineage-specific phenomenon in which basal-like tumors, HER2-related tumors with high hypoxia, as well as normal basal epithelial cells express increased mRNA levels of HIF-1$\alpha$ compared to luminal types and silencing of HIF-1$\alpha$ results in decreased expression of hypoxia-induced genes.$\backslash$n$\backslash$nCONCLUSIONS: This study demonstrates differences in microenvironmental conditions in HER2-related subgroups defined by distinct oncogenic pathway activities, and provides a mechanistic explanation for differences in the observed hypoxia response between these subgroups. Collectively, these data demonstrate the potential of a pathway-based classification strategy as a framework to integrate genetic and non-genetic factors to investigate the basis of tumor heterogeneity.},
author = {Gatza, Michael L and Kung, Hsiu-Ni and Blackwell, Kimberly L and Dewhirst, Mark W and Marks, Jeffrey R and Chi, Jen-Tsan},
doi = {10.1186/bcr2899},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Gatza et al.{\_}2011{\_}Analysis of tumor environmental response and oncogenic pathway activation identifies distinct basal and luminal featur.pdf:pdf},
issn = {1465-5411},
journal = {Breast Cancer Res.},
number = {3},
pages = {R62},
pmid = {21672245},
publisher = {BioMed Central Ltd},
title = {{Analysis of tumor environmental response and oncogenic pathway activation identifies distinct basal and luminal features in HER2-related breast tumor subtypes}},
volume = {13},
year = {2011}
}
@article{Tatemoto1982,
abstract = {2915},
author = {Tatemoto, K and Carlquist, M and Mutt, V},
doi = {10.1038/296659a0},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Tatemoto, Carlquist, Mutt - 1982 - Neuropeptide Y--a novel brain peptide with structural similarities to peptide YY and pancreatic polyp.pdf:pdf},
isbn = {0028-0836 (Print) 0028-0836 (Linking)},
issn = {0028-0836},
journal = {Nature},
keywords = {obesity},
mendeley-tags = {obesity},
pages = {659--660},
pmid = {6896083},
title = {{Neuropeptide Y--a novel brain peptide with structural similarities to peptide YY and pancreatic polypeptide.}},
volume = {296},
year = {1982}
}
@article{Tomasetti2014,
author = {Tomasetti, Cristian and Vogelstein, Bert},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Tomasetti, Vogelstein - 2015 - Variation in cancer risk among tissues can be explained by the number of stem cell divisions.pdf:pdf},
journal = {Science (80-. ).},
keywords = {cancer,environmental factors},
mendeley-tags = {cancer,environmental factors},
number = {6217},
pages = {78--81},
title = {{Variation in cancer risk among tissues can be explained by the number of stem cell divisions}},
volume = {347},
year = {2015}
}
@article{Jackson1997,
author = {Jackson, Robert S. and Creemers, John W M and Ohagi, Shinya and Raffin-Sanson, Marie-Laure and Sanders, Louise and Montague, Carl T and Hutton, John C. and O'Rahilly, Stephen},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Jackson et al. - 1997 - Obesity and impaired prohormone processing associated with mutations in the human prohormone convertase 1 gene.pdf:pdf},
journal = {Nat. Genet.},
keywords = {obesity},
mendeley-tags = {obesity},
pages = {303--306},
pmid = {8985244},
title = {{Obesity and impaired prohormone processing associated with mutations in the human prohormone convertase 1 gene}},
volume = {16},
year = {1997}
}
@article{Moustafa2013,
abstract = {Obesity is a disorder characterized by an excess accumulation of body fat resulting from a mismatch between energy intake and expenditure. Incidence of obesity has increased dramatically in the past few years, almost certainly fuelled by a shift in dietary habits owing to the widespread availability of low-cost, hypercaloric foods. However, clear differences exist in obesity susceptibility among individuals exposed to the same obesogenic environment, implicating genetic risk factors. Numerous genes have been shown to be involved in the development of monofactorial forms of obesity. In genome-wide association studies, a large number of common variants have been associated with adiposity levels, each accounting for only a small proportion of the predicted heritability. Although the small effect sizes of obesity variants identified in genome-wide association studies currently preclude their utility in clinical settings, screening for a number of monogenic obesity variants is now possible. Such regular screening will provide more informed prognoses and help in the identification of at-risk individuals who could benefit from early intervention, in evaluation of the outcomes of current obesity treatments, and in personalization of the clinical management of obesity. This Review summarizes current advances in obesity genetics and discusses the future of research in this field and the potential relevance to personalized obesity therapy.},
author = {{El-Sayed Moustafa}, Julia S and Froguel, Philippe},
doi = {10.1038/nrendo.2013.57},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/El-Sayed Moustafa, Froguel - 2013 - From obesity genetics to the future of personalized obesity therapy.pdf:pdf},
isbn = {1759-5037 (Electronic)$\backslash$r1759-5029 (Linking)},
issn = {1759-5037},
journal = {Nat. Rev. Endocrinol.},
keywords = {Animals,Body Mass Index,Genetic Predisposition to Disease,Genetic Predisposition to Disease: genetics,Humans,Obesity,Obesity: diagnosis,Obesity: genetics,obesity},
mendeley-tags = {obesity},
number = {7},
pages = {402--413},
pmid = {23529041},
publisher = {Nature Publishing Group},
title = {{From obesity genetics to the future of personalized obesity therapy.}},
volume = {9},
year = {2013}
}
@article{Swinburn2011,
abstract = {The simultaneous increases in obesity in almost all countries seem to be driven mainly by changes in the global food system, which is producing more processed, affordable, and effectively marketed food than ever before. This passive overconsumption of energy leading to obesity is a predictable outcome of market economies predicated on consumption-based growth. The global food system drivers interact with local environmental factors to create a wide variation in obesity prevalence between populations. Within populations, the interactions between environmental and individual factors, including genetic makeup, explain variability in body size between individuals. However, even with this individual variation, the epidemic has predictable patterns in subpopulations. In low-income countries, obesity mostly affects middle-aged adults (especially women) from wealthy, urban environments; whereas in high-income countries it affects both sexes and all ages, but is disproportionately greater in disadvantaged groups. Unlike other major causes of preventable death and disability, such as tobacco use, injuries, and infectious diseases, there are no exemplar populations in which the obesity epidemic has been reversed by public health measures. This absence increases the urgency for evidence-creating policy action, with a priority on reduction of the supply-side drivers. ?? 2011 Elsevier Ltd.},
author = {Swinburn, Boyd A. and Sacks, Gary and Hall, Kevin D. and McPherson, Klim and Finegood, Diane T. and Moodie, Marjory L. and Gortmaker, Steven L.},
doi = {10.1016/S0140-6736(11)60813-1},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Swinburn et al. - 2011 - The global obesity pandemic Shaped by global drivers and local environments.pdf:pdf},
isbn = {01406736},
issn = {01406736},
journal = {Lancet},
keywords = {obesity},
mendeley-tags = {obesity},
number = {9793},
pages = {804--814},
pmid = {21872749},
title = {{The global obesity pandemic: Shaped by global drivers and local environments}},
volume = {378},
year = {2011}
}
@article{Lashinger2014,
author = {Lashinger, L M and Rossi, E L and Hursting, S D},
doi = {10.1038/clpt.2014.136},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Lashinger, Rossi, Hursting{\_}2014{\_}Obesity and Resistance to Cancer Chemotherapy Interacting Roles of Inflammation and Metabolic Dysregulat.pdf:pdf},
issn = {0009-9236},
journal = {Clin. Pharmacol. Ther.},
number = {4},
pages = {458--463},
title = {{Obesity and Resistance to Cancer Chemotherapy: Interacting Roles of Inflammation and Metabolic Dysregulation}},
volume = {96},
year = {2014}
}
@article{Clement1998,
abstract = {The adipocyte-specific hormone leptin, the product of the obese (ob) gene, regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure. Leptin acts through the leptin receptor, a single-transmembrane-domain receptor of the cytokine-receptor family. In rodents, homozygous mutations in genes encoding leptin or the leptin receptor cause early-onset morbid obesity, hyperphagia and reduced energy expenditure. These rodents also show hypercortisolaemia, alterations in glucose homeostasis, dyslipidaemia, and infertility due to hypogonadotropic hypogonadisms. In humans, leptin deficiency due to a mutation in the leptin gene is associated with early-onset obesity. Here we describe a homozygous mutation in the human leptin receptor gene that results in a truncated leptin receptor lacking both the transmembrane and the intracellular domains. In addition to their early-onset morbid obesity, patients homozygous for this mutation have no pubertal development and their secretion of growth hormone and thyrotropin is reduced. These results indicate that leptin is an important physiological regulator of several endocrine functions in humans.},
archivePrefix = {arXiv},
arxivId = {NIHMS150003},
author = {Clement, K and Vaisse, C and Lahlou, N and Cabrol, S and Pelloux, V and Cassuto, D and Gourmelen, M and Dina, C and Chambaz, J and Lacorte, J M and Basdevant, A and Bougneres, P and Lebouc, Y and Froguel, P and Guy-Grand, B},
doi = {10.1038/32911},
eprint = {NIHMS150003},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Clement et al. - 1998 - A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction.pdf:pdf},
isbn = {0028-0836 (Print)$\backslash$r0028-0836 (Linking)},
issn = {0028-0836},
journal = {Nature},
keywords = {*Mutation,*Receptors, Cell Surface,Adult,Body Height,Body Weight,Carrier Proteins/*genetics/physiology,Cell Surface,Family Health,Female,Genotype,Homozygote,Human Growth Hormone/secretion,Humans,Leptin,Male,Messenger/metabolism,Obesity/*genetics,Pituitary Diseases/*genetics/physiopathology,Polymorphism, Single-Stranded Conformational,RNA, Messenger/metabolism,Receptors, Leptin,Single-Stranded Conformational,obesity},
mendeley-tags = {obesity},
number = {6674},
pages = {398--401},
pmid = {9537324},
title = {{A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction}},
volume = {392},
year = {1998}
}
@article{Clark1984,
author = {Clark, John T and Kalra, Pushpa S and Crowley, William R and Kalra, Satya P},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Clark et al. - 1984 - Neuropeptide Y and human pancreatic polypeptide stimulate feeding behavior in rats.pdf:pdf},
journal = {Endocrinology},
keywords = {obesity},
mendeley-tags = {obesity},
number = {1},
pages = {427--429},
title = {{Neuropeptide Y and human pancreatic polypeptide stimulate feeding behavior in rats}},
volume = {115},
year = {1984}
}
@article{Fidler2003,
abstract = {Researchers have been studying metastasis for more than 100 years, and only recently have we gained insight into the mechanisms by which metastatic cells arise from primary tumours and the reasons that certain tumour types tend to metastasize to specific organs. Stephen Paget's 1889 proposal that metastasis depends on cross-talk between selected cancer cells (the 'seeds') and specific organ microenvironments (the 'soil') still holds forth today. It is now known that the potential of a tumour cell to metastasize depends on its interactions with the homeostatic factors that promote tumour-cell growth, survival, angiogenesis, invasion and metastasis. How has this field developed over the past century, and what major breakthroughs are most likely to lead to effective therapeutic approaches?},
author = {Fidler, Isaiah J},
doi = {10.1038/nrc1098},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Fidler - 2003 - The pathogenesis of cancer metastasis the 'seed and soil' hypothesis revisited.pdf:pdf},
isbn = {1474-175X (Print)$\backslash$n1474-175X (Linking)},
issn = {1474175X},
journal = {Nat. Rev. Cancer},
keywords = {cancer,metastasis},
mendeley-tags = {cancer,metastasis},
number = {6},
pages = {453--458},
pmid = {12778135},
title = {{The pathogenesis of cancer metastasis: the 'seed and soil' hypothesis revisited}},
volume = {3},
year = {2003}
}
@article{Joshi2005,
abstract = {Reactome, located at http://www.reactome.org is a curated, peer-reviewed resource of human biological processes. Given the genetic makeup of an organism, the complete set of possible reactions constitutes its reactome. The basic unit of the Reactome database is a reaction; reactions are then grouped into causal chains to form pathways. The Reactome data model allows us to represent many diverse processes in the human system, including the pathways of intermediary metabolism, regulatory pathways, and signal transduction, and high-level processes, such as the cell cycle. Reactome provides a qualitative framework, on which quantitative data can be superimposed. Tools have been developed to facilitate custom data entry and annotation by expert biologists, and to allow visualization and exploration of the finished dataset as an interactive process map. Although our primary curational domain is pathways from Homo sapiens, we regularly create electronic projections of human pathways onto other organisms via putative orthologs, thus making Reactome relevant to model organism research communities. The database is publicly available under open source terms, which allows both its content and its software infrastructure to be freely used and redistributed.},
author = {Joshi-Tope, G. and Gillespie, M. and Vastrik, I. and D{\&}apos;Eustachio, P. and Schmidt, E. and de Bono, B. and Jassal, B. and Gopinath, G. R. and Wu, G. R. and Matthews, L. and Lewis, S. and Birney, E. and Stein, L.},
doi = {10.1093/nar/gki072},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Joshi-Tope et al. - 2005 - Reactome A knowledgebase of biological pathways.pdf:pdf},
isbn = {1362-4962 (Electronic)$\backslash$r0305-1048 (Linking)},
issn = {03051048},
journal = {Nucleic Acids Res.},
number = {DATABASE ISS.},
pages = {D428--D432},
pmid = {15608231},
title = {{Reactome: A knowledgebase of biological pathways}},
volume = {33},
year = {2005}
}
@article{WHO2014,
abstract = {Description of the global burden of NCDs, their risk factors and determinants},
author = {{World Health Organisation}},
doi = {ISBN 9789241564854},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/World Health Organisation - 2014 - Global status report on noncommunicable diseases 2014.pdf:pdf},
isbn = {978 92 4 156485 4},
journal = {Geneva World Heal. Organ.},
keywords = {obesity},
mendeley-tags = {obesity},
title = {{Global status report on noncommunicable diseases 2014}},
year = {2014}
}
@article{Liu2009,
abstract = {The phosphoinositide 3-kinase (PI3K) pathway, a critical signal transduction system linking oncogenes and multiple receptor classes to many essential cellular functions, is perhaps the most commonly activated signaling pathway in human cancer. This pathway thus presents both an opportunity and a challenge for cancer therapy. Even as inhibitors that target PI3K isoforms and other major nodes in the pathway including AKT and mTOR reach clinical trials, major issues remain. Here we highlight recent progress made in our understanding of the PI3K pathway and discuss both the promises and challenges for the therapeutic development of agents targeting the PI3K pathway in cancer.},
author = {Liu, Pixu and Cheng, Hailing and Roberts, Thomas M and Zhao, Jean J},
doi = {10.1038/nrd2926},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Liu et al. - 2009 - Targeting the phosphoinositide 3-kinase (PI3K) pathway in cancer.pdf:pdf},
isbn = {1474-1784 (Electronic)},
issn = {1474-1776},
journal = {Nat. Rev. Drug Discov.},
keywords = {PI3K,cancer},
mendeley-tags = {PI3K,cancer},
number = {8},
pages = {627--644},
pmid = {19644473},
publisher = {Nature Publishing Group},
title = {{Targeting the phosphoinositide 3-kinase (PI3K) pathway in cancer}},
volume = {8},
year = {2009}
}
@article{Franks2010,
author = {Franks, Paul W. and Hanson, Robert L. and Knowler, William C. and Sievers, Maurice L. and Bennett, Peter H. and Looker, Helen C.},
doi = {10.1056/NEJMoa0810625)},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Franks et al. - 2010 - Childhood obesity, other cardiovascular risk factors, and premature death.pdf:pdf},
journal = {N. Engl. J. Med.},
keywords = {obesity},
mendeley-tags = {obesity},
number = {6},
pages = {485--493},
title = {{Childhood obesity, other cardiovascular risk factors, and premature death}},
volume = {362},
year = {2010}
}
@article{Chang2013,
abstract = {The Cancer Genome Atlas (TCGA) Research Network has profiled and analyzed large numbers of human tumors to discover molecular aberrations at the DNA, RNA, protein and epigenetic levels. The resulting rich data provide a major opportunity to develop an integrated picture of commonalities, differences and emergent themes across tumor lineages. The Pan-Cancer initiative compares the first 12 tumor types profiled by TCGA. Analysis of the molecular aberrations and their functional roles across tumor types will teach us how to extend therapies effective in one cancer type to others with a similar genomic profile.},
author = {Chang, Kyle and Creighton, Chad J and Davis, Caleb and Donehower, Lawrence and Drummond, Jennifer and Wheeler, David and Ally, Adrian and Balasundaram, Miruna and Birol, Inanc and Butterfield, Yaron S N and Chu, Andy and Chuah, Eric and Chun, Hye-Jung E and Dhalla, Noreen and Guin, Ranabir and Hirst, Martin and Hirst, Carrie and Holt, Robert A and Jones, Steven J M and Lee, Darlene and Li, Haiyan I and Marra, Marco A and Mayo, Michael and Moore, Richard A and Mungall, Andrew J and Robertson, A Gordon and Schein, Jacqueline E and Sipahimalani, Payal and Tam, Angela and Thiessen, Nina and Varhol, Richard J and Beroukhim, Rameen and Bhatt, Ami S and Brooks, Angela N and Cherniack, Andrew D and Freeman, Samuel S and Gabriel, Stacey B and Helman, Elena and Jung, Joonil and Meyerson, Matthew and Ojesina, Akinyemi I and Pedamallu, Chandra Sekhar and Saksena, Gordon and Schumacher, Steven E and Tabak, Barbara and Zack, Travis and Lander, Eric S and Bristow, Christopher A and Hadjipanayis, Angela and Haseley, Psalm and Kucherlapati, Raju and Lee, Semin and Lee, Eunjung and Luquette, Lovelace J and Mahadeshwar, Harshad S and Pantazi, Angeliki and Parfenov, Michael and Park, Peter J and Protopopov, Alexei and Ren, Xiaojia and Santoso, Netty and Seidman, Jonathan and Seth, Sahil and Song, Xingzhi and Tang, Jiabin and Xi, Ruibin and Xu, Andrew W and Yang, Lixing and Zeng, Dong and Auman, J Todd and Balu, Saianand and Buda, Elizabeth and Fan, Cheng and Hoadley, Katherine A and Jones, Corbin D and Meng, Shaowu and Mieczkowski, Piotr A and Parker, Joel S and Perou, Charles M and Roach, Jeffrey and Shi, Yan and Silva, Grace O and Tan, Donghui and Veluvolu, Umadevi and Waring, Scot and Wilkerson, Matthew D and Wu, Junyuan and Zhao, Wei and Bodenheimer, Tom and Hayes, D Neil and Hoyle, Alan P and Jeffreys, Stuart R and Mose, Lisle E and Simons, Janae V and Soloway, Mathew G and Baylin, Stephen B and Berman, Benjamin P and Bootwalla, Moiz S and Danilova, Ludmila and Herman, James G and Hinoue, Toshinori and Laird, Peter W and Rhie, Suhn K and Shen, Hui and Triche, Timothy and Weisenberger, Daniel J and Carter, Scott L and Cibulskis, Kristian and Chin, Lynda and Zhang, Jianhua and Getz, Gad and Sougnez, Carrie and Wang, Min and Dinh, Huyen and Doddapaneni, Harsha Vardhan and Gibbs, Richard and Gunaratne, Preethi and Han, Yi and Kalra, Divya and Kovar, Christie and Lewis, Lora and Morgan, Margaret and Morton, Donna and Muzny, Donna and Reid, Jeffrey and Xi, Liu and Cho, Juok and Dicara, Daniel and Frazer, Scott and Gehlenborg, Nils and Heiman, David I and Kim, Jaegil and Lawrence, Michael S and Lin, Pei and Liu, Yingchun and Noble, Michael S and Stojanov, Petar and Voet, Doug and Zhang, Hailei and Zou, Lihua and Stewart, Chip and Bernard, Brady and Bressler, Ryan and Eakin, Andrea and Iype, Lisa and Knijnenburg, Theo and Kramer, Roger and Kreisberg, Richard and Leinonen, Kalle and Lin, Jake and Liu, Yuexin and Miller, Michael and Reynolds, Sheila M and Rovira, Hector and Shmulevich, Ilya and Thorsson, Vesteinn and Yang, Da and Zhang, Wei and Amin, Samirkumar and Wu, Chang-Jiun and Wu, Chia-Chin and Akbani, Rehan and Aldape, Kenneth and Baggerly, Keith A and Broom, Bradley and Casasent, Tod D and Cleland, James and Creighton, Chad and Dodda, Deepti and Edgerton, Mary and Han, Leng and Herbrich, Shelley M and Ju, Zhenlin and Kim, Hoon and Lerner, Seth and Li, Jun and Liang, Han and Liu, Wenbin and Lorenzi, Philip L and Lu, Yiling and Melott, James and Mills, Gordon B and Nguyen, Lam and Su, Xiaoping and Verhaak, Roeland and Wang, Wenyi and Weinstein, John N and Wong, Andrew and Yang, Yang and Yao, Jun and Yao, Rong and Yoshihara, Kosuke and Yuan, Yuan and Yung, Alfred K and Zhang, Nianxiang and Zheng, Siyuan and Ryan, Michael and Kane, David W and Aksoy, B Arman and Ciriello, Giovanni and Dresdner, Gideon and Gao, Jianjiong and Gross, Benjamin and Jacobsen, Anders and Kahles, Andre and Ladanyi, Marc and Lee, William and Lehmann, Kjong-Van and Miller, Martin L and Ramirez, Ricardo and R{\"{a}}tsch, Gunnar and Reva, Boris and Sander, Chris and Schultz, Nikolaus and Senbabaoglu, Yasin and Shen, Ronglai and Sinha, Rileen and Sumer, S Onur and Sun, Yichao and Taylor, Barry S and Weinhold, Nils and Fei, Suzanne and Spellman, Paul and Benz, Christopher and Carlin, Daniel and Cline, Melisssa and Craft, Brian and Ellrott, Kyle and Goldman, Mary and Haussler, David and Ma, Singer and Ng, Sam and Paull, Evan and Radenbaugh, Amie and Salama, Sofie and Sokolov, Artem and Stuart, Joshua M and Swatloski, Teresa and Uzunangelov, Vladislav and Waltman, Peter and Yau, Christina and Zhu, Jing and Hamilton, Stanley R and Abbott, Scott and Abbott, Rachel and Dees, Nathan D and Delehaunty, Kim and Ding, Li and Dooling, David J and Eldred, Jim M and Fronick, Catrina C and Fulton, Robert and Fulton, Lucinda L and Kalicki-Veizer, Joelle and Kanchi, Krishna-Latha and Kandoth, Cyriac and Koboldt, Daniel C and Larson, David E and Ley, Timothy J and Lin, Ling and Lu, Charles and Magrini, Vincent J and Mardis, Elaine R and McLellan, Michael D and McMichael, Joshua F and Miller, Christopher A and O'Laughlin, Michelle and Pohl, Craig and Schmidt, Heather and Smith, Scott M and Walker, Jason and Wallis, John W and Wendl, Michael C and Wilson, Richard K and Wylie, Todd and Zhang, Qunyuan and Burton, Robert and Jensen, Mark A and Kahn, Ari and Pihl, Todd and Pot, David and Wan, Yunhu and Levine, Douglas A and Black, Aaron D and Bowen, Jay and Frick, Jessica and Gastier-Foster, Julie M and Harper, Hollie A and Helsel, Carmen and Leraas, Kristen M and Lichtenberg, Tara M and McAllister, Cynthia and Ramirez, Nilsa C and Sharpe, Samantha and Wise, Lisa and Zmuda, Erik and Chanock, Stephen J and Davidsen, Tanja and Demchok, John A and Eley, Greg and Felau, Ina and Ozenberger, Brad A and Sheth, Margi and Sofia, Heidi and Staudt, Louis and Tarnuzzer, Roy and Wang, Zhining and Yang, Liming and Zhang, Jiashan and Omberg, Larsson and Margolin, Adam and Raphael, Benjamin J and Vandin, Fabio and Wu, Hsin-Ta and Leiserson, Mark D M and Benz, Stephen C and Vaske, Charles J and Noushmehr, Houtan and Wolf, Denise and Veer, Laura Van't and Collisson, Eric A and Anastassiou, Dimitris and {Ou Yang}, Tai-Hsien and Lopez-Bigas, Nuria and Gonzalez-Perez, Abel and Tamborero, David and Xia, Zheng and Li, Wei and Cho, Dong-Yeon and Przytycka, Teresa and Hamilton, Mark and McGuire, Sean and Nelander, Sven and Johansson, Patrik and J{\"{o}}rnsten, Rebecka and Kling, Teresia and Sanchez, Jose and Shaw, Kenna R Mills},
doi = {10.1038/ng.2764},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Chang et al.{\_}2013{\_}The Cancer Genome Atlas Pan-Cancer analysis project.pdf:pdf},
isbn = {doi:10.1038/ng.2764},
issn = {1546-1718},
journal = {Nat. Genet.},
number = {10},
pages = {1113--1120},
pmid = {24071849},
publisher = {Nature Publishing Group},
title = {{The Cancer Genome Atlas Pan-Cancer analysis project.}},
volume = {45},
year = {2013}
}
@misc{hgu133,
author = {Carlson, M},
title = {{hgu133a.db: Affymetrix Human Genome U133 Set annotation data (chip hgu133a). R package version 3.2.3}},
year = {2016}
}
@article{West2001,
abstract = {Prognostic and predictive factors are indispensable tools in the treatment of patients with neoplastic disease. For the most part, such factors rely on a few specific cell surface, histological, or gross pathologic features. Gene expression assays have the potential to supplement what were previously a few distinct features with many thousands of features. We have developed Bayesian regression models that provide predictive capability based on gene expression data derived from DNA microarray analysis of a series of primary breast cancer samples. These patterns have the capacity to discriminate breast tumors on the basis of estrogen receptor status and also on the categorized lymph node status. Importantly, we assess the utility and validity of such models in predicting the status of tumors in crossvalidation determinations. The practical value of such approaches relies on the ability not only to assess relative probabilities of clinical outcomes for future samples but also to provide an honest assessment of the uncertainties associated with such predictive classifications on the basis of the selection of gene subsets for each validation analysis. This latter point is of critical importance in the ability to apply these methodologies to clinical assessment of tumor phenotype.},
author = {West, M and Blanchette, C and Dressman, H and Huang, E and Ishida, S and Spang, R and Zuzan, H and Olson, J A and Marks, J R and Nevins, J R},
doi = {10.1073/pnas.201162998},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/West et al. - 2001 - Predicting the clinical status of human breast cancer by using gene expression profiles.pdf:pdf},
isbn = {0027-8424 LA - eng},
issn = {0027-8424},
journal = {Proc. Natl. Acad. Sci. U. S. A.},
keywords = {Bacillus anthracis,Breast Neoplasms,Breast Neoplasms: enzymology,Breast Neoplasms: genetics,Breast Neoplasms: pathology,Breast Neoplasms: surgery,Enzymes,Enzymes: genetics,Estrogen,Estrogen: analysis,Female,Humans,Lymph Node Excision,Lymph Nodes,Lymph Nodes: pathology,Multigene Family,Oligonucleotide Array Sequence Analysis,Phenotype,Predictive Value of Tests,Probability,Receptors,Reproducibility of Results},
number = {20},
pages = {11462--11467},
pmid = {11562467},
title = {{Predicting the clinical status of human breast cancer by using gene expression profiles.}},
volume = {98},
year = {2001}
}
@article{Zimmermann1999a,
abstract = {Activation of the protein kinase Raf can lead to opposing cellular responses such as proliferation, growth arrest, apoptosis, or differentiation. Akt (protein kinase B), a member of a different signaling pathway that also regulates these responses, interacted with Raf and phosphorylated this protein at a highly conserved serine residue in its regulatory domain in vivo. This phosphorylation of Raf by Akt inhibited activation of the Raf-MEK-ERK signaling pathway and shifted the cellular response in a human breast cancer cell line from cell cycle arrest to proliferation. These observations provide a molecular basis for cross talk between two signaling pathways at the level of Raf and Akt.},
author = {Zimmermann, S and Moelling, K},
doi = {10.1126/science.286.5445.1741},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Zimmermann, Moelling - 1999 - Phosphorylation and regulation of Raf by Akt (protein kinase B).pdf:pdf},
isbn = {0036-8075 (Print)0036-8075},
issn = {00368075},
journal = {Science},
keywords = {*Cell Division,*MAP Kinase Signaling System,Cell Line,Chromones/pharmacology,Cultured,Cyclin-Dependent Kinase Inhibitor p21,Cyclins/metabolism,Enzyme Activation,Enzyme Inhibitors/pharmacology,Epidermal Growth Factor/pharmacology,Flavonoids/pharmacology,Humans,Morpholines/pharmacology,Phosphatidylinositol 3-Kinases/antagonists {\&} inhib,Phosphorylation,Phosphoserine/metabolism,Protein-Serine-Threonine Kinases/antagonists {\&} inh,Proto-Oncogene Proteins c-akt,Proto-Oncogene Proteins c-raf/antagonists {\&} inhibi,Proto-Oncogene Proteins/antagonists {\&} inhibitors/*,Raf/Akt crosstalk,Recombinant Fusion Proteins/metabolism,Signal Transduction,Somatomedins/pharmacology,Tetradecanoylphorbol Acetate/pharmacology,Tumor Cells,cancer,ras Proteins/metabolism},
mendeley-tags = {Raf/Akt crosstalk,cancer},
number = {5445},
pages = {1741--1744},
pmid = {10576742},
title = {{Phosphorylation and regulation of Raf by Akt (protein kinase B)}},
volume = {286},
year = {1999}
}
@article{Mokdad2003,
author = {Mokdad, Ali H and Ford, Earl S and Bowman, Barbara A and Dietz, William H and Vinicor, Frank and Bales, Virginia S and Marks, James S},
doi = {10.1001/jama.289.1.76},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Mokdad et al. - 2003 - Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001.pdf:pdf},
isbn = {0098-7484 (Print)},
issn = {0098-7484},
journal = {Jama},
keywords = {Diabetes Mellitus,Endocrine Diseases,Obesity,Public Health},
pages = {76--79},
pmid = {12503980},
title = {{Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001}},
volume = {289},
year = {2003}
}
@book{Hochberg1987,
address = {New York},
author = {Hochberg, Yosef and Tamhane, Ajit C.},
publisher = {John Wiley and Sons},
title = {{Multiple comparison procedures}},
year = {1987}
}
@article{Futreal2004,
abstract = {A central aim of cancer research has been to identify the mutated genes that are causally implicated in oncogenesis (‘cancer genes'). After two decades of searching, how many have been identified and how do they compare to the complete gene set that has been revealed by the human genome sequence? We have conducted a ‘census' of cancer genes that indicates that mutations in more than 1{\%} of genes contribute to human cancer. The census illustrates striking features in the types of sequence alteration, cancer classes in which oncogenic mutations have been identified and protein domains that are encoded by cancer genes.},
author = {Futreal, P.a. Andrew and Coin, Lachlan and Marshall, Mhairi and Down, Thomas and Hubbard, Timothy and Wooster, Richard and Rahman, Nazneen and Stratton, Michael R. M.R.},
doi = {10.1038/nrc1299.A},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Futreal et al. - 2004 - A census of human cancer genes.pdf:pdf},
isbn = {1474-175X (Print)$\backslash$r1474-175X (Linking)},
issn = {1474-175X},
journal = {Nat. Rev. Cancer},
keywords = {cancer,genes and mutations,review},
mendeley-tags = {cancer,genes and mutations,review},
number = {3},
pages = {177--183},
pmid = {14993899},
title = {{A census of human cancer genes}},
volume = {4},
year = {2004}
}
@article{Saltiel2002,
abstract = {Despite remarkable progress in dissecting the signaling pathways that are crucial for the metabolic effects of insulin, the molecular basis for the specificity of its cellular actions is not fully understood. One clue might lie in the spatial and temporal aspects of signaling. Recent evidence suggests that signaling molecules and pathways are localized to discrete compartments in cells by specific protein interactions. Also, the rapid termination of tyrosine or lipid phosphorylation by phosphatases or serine kinases might tightly control the strength of a signaling pathway, thus determining its effect on growth, differentiation and metabolism.},
author = {Saltiel, Alan R. and Pessin, Jeffrey E.},
doi = {10.1016/S0962-8924(01)02207-3},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Saltiel, Pessin - 2002 - Insulin signaling pathways in time and space.pdf:pdf},
isbn = {0962-8924 (Print)$\backslash$r0962-8924 (Linking)},
issn = {09628924},
journal = {Trends Cell Biol.},
keywords = {insulin},
mendeley-tags = {insulin},
number = {2},
pages = {65--71},
pmid = {11849969},
title = {{Insulin signaling pathways in time and space}},
volume = {12},
year = {2002}
}
@article{Smyth2004,
abstract = {The problem of identifying differentially expressed genes in designed microarray experiments is considered. Lonnstedt and Speed (2002) derived an expression for the posterior odds of differential expression in a replicated two-color experiment using a simple hierarchical parametric model. The purpose of this paper is to develop the hierarchical model of Lonnstedt and Speed (2002) into a practical approach for general microarray experiments with arbitrary numbers of treatments and RNA samples. The model is reset in the context of general linear models with arbitrary coefficients and contrasts of interest. The approach applies equally well to both single channel and two color microarray experiments. Consistent, closed form estimators are derived for the hyperparameters in the model. The estimators proposed have robust behavior even for small numbers of arrays and allow for incomplete data arising from spot filtering or spot quality weights. The posterior odds statistic is reformulated in terms of a moderated t-statistic in which posterior residual standard deviations are used in place of ordinary standard deviations. The empirical Bayes approach is equivalent to shrinkage of the estimated sample variances towards a pooled estimate, resulting in far more stable inference when the number of arrays is small. The use of moderated t-statistics has the advantage over the posterior odds that the number of hyperparameters which need to estimated is reduced; in particular, knowledge of the non-null prior for the fold changes are not required. The moderated t-statistic is shown to follow a t-distribution with augmented degrees of freedom. The moderated t inferential approach extends to accommodate tests of composite null hypotheses through the use of moderated F-statistics. The performance of the methods is demonstrated in a simulation study. Results are presented for two publicly available data sets.},
author = {Smyth, Gordon K},
doi = {10.2202/1544-6115.1027},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Smyth - 2004 - Linear Models and Empirical Bayes Methods for Assessing Differential Expression in Microarray Experiments Linear Models a.pdf:pdf},
isbn = {1544-6115; 1544-6115},
issn = {1544-6115},
journal = {Stat. Appl. Genet. Mol. Biol.},
number = {1},
pages = {1--26},
pmid = {16646809},
title = {{Linear Models and Empirical Bayes Methods for Assessing Differential Expression in Microarray Experiments Linear Models and Empirical Bayes Methods for Assessing Differential Expression in Microarray Experiments}},
volume = {3},
year = {2004}
}
@article{Challis2002,
abstract = {The functional loss of both alleles of the human pro-opiomelanocortin (POMC) gene leads to a very rare syndrome of hypoadrenalism, red hair and early-onset obesity. In order to examine whether more subtle genetic variants in POMC might contribute to early-onset obesity, the coding region of the gene was sequenced in 262 Caucasian subjects with a history of severe obesity from childhood. Two children were found to be heterozygous for a missense mutation, R236G, which disrupts the dibasic cleavage site between beta melanocyte-stimulating hormone (beta-MSH) and beta-endorphin. Beta-TC3 cells transfected with the mutant POMC cDNA produced a mutant beta-MSH/beta-endorphin fusion protein. This fusion protein bound to the human melanocortin-4 receptor (hMC4R) with an affinity similar to its natural ligands, but had a markedly reduced ability to activate the receptor. This variant co-segregated with early-onset obesity over three generations in one family and was absent in 412 normal weight UK Caucasian controls. Combining the results in UK Caucasians with a new case-control study in French subjects and three previously published reports, mutations disrupting this processing site were present in 0.88{\%} of subjects with early-onset obesity and 0.22{\%} of normal-weight controls. These results suggest that the R236G mutation may confer an inherited susceptibility to obesity through the production of an aberrant fusion protein that has the capacity to interfere with central melanocortin signalling.},
author = {Challis, Benjamin G and Pritchard, Lynn E and Creemers, John W M and Delplanque, Jerome and Keogh, Julia M and Luan, Jian'an and Wareham, Nicholas J and Yeo, Giles S H and Bhattacharyya, Sumit and Froguel, Phillipe and White, Anne and Farooqi, I Sadaf and O'Rahilly, Stephen},
doi = {10.1186/1746-6148-8-111},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Challis et al. - 2002 - A missense mutation disrupting a dibasic prohormone processing site in pro-opiomelanocortin (POMC) increases sus.pdf:pdf},
isbn = {0964-6906 (Print)$\backslash$n0964-6906 (Linking)},
issn = {0964-6906},
journal = {Hum. Mol. Genet.},
keywords = {Adolescent,Adrenal Insufficiency,Adrenal Insufficiency: genetics,Animals,CHO Cells,Case-Control Studies,Corticotropin,Corticotropin: metabolism,Cricetinae,DNA Mutational Analysis,DNA Primers,DNA Primers: chemistry,Disease Susceptibility,Female,Hair Color,Hair Color: genetics,Humans,Male,Melanocortin,Missense,Missense: genetics,Mutation,Obesity,Obesity: etiology,Obesity: genetics,Pedigree,Peptide Fragments,Peptide Fragments: chemical synthesis,Peptide Fragments: metabolism,Polymerase Chain Reaction,Polymorphism,Precipitin Tests,Pro-Opiomelanocortin,Pro-Opiomelanocortin: genetics,Receptor,Receptors,Recombinant Fusion Proteins,Recombinant Fusion Proteins: metabolism,Restriction Fragment Length,Type 4,beta-Endorphin,beta-Endorphin: metabolism,beta-MSH,beta-MSH: metabolism,obesity},
mendeley-tags = {obesity},
number = {17},
pages = {1997--2004},
pmid = {12165561},
title = {{A missense mutation disrupting a dibasic prohormone processing site in pro-opiomelanocortin (POMC) increases susceptibility to early-onset obesity through a novel molecular mechanism.}},
volume = {11},
year = {2002}
}
@article{Subramanian2005,
abstract = {Although genomewide RNA expression analysis has become a routine tool in biomedical research, extracting biological insight from such information remains a major challenge. Here, we describe a powerful analytical method called Gene Set Enrichment Analysis (GSEA) for interpreting gene expression data. The method derives its power by focusing on gene sets, that is, groups of genes that share common biological function, chromosomal location, or regulation. We demonstrate how GSEA yields insights into several cancer-related data sets, including leukemia and lung cancer. Notably, where single-gene analysis finds little similarity between two independent studies of patient survival in lung cancer, GSEA reveals many biological pathways in common. The GSEA method is embodied in a freely available software package, together with an initial database of 1,325 biologically defined gene sets.},
author = {Subramanian, Aravind and Tamayo, Pablo and Mootha, Vamsi K and Mukherjee, Sayan and Ebert, Benjamin L and Gillette, Michael a and Paulovich, Amanda and Pomeroy, Scott L and Golub, Todd R and Lander, Eric S and Mesirov, Jill P},
doi = {10.1073/pnas.0506580102},
file = {:Users/rikutakei/Downloads/papers/PNAS-2005-Subramanian-15545-50.pdf:pdf},
isbn = {0027-8424 (Print)$\backslash$r0027-8424 (Linking)},
issn = {0027-8424},
journal = {Proc. Natl. Acad. Sci. U. S. A.},
keywords = {Acute,Acute: genetics,Cell Line,Female,Gene Expression Profiling,Gene Expression Profiling: methods,Genes,Genome,Humans,Leukemia,Lung Neoplasms,Lung Neoplasms: genetics,Lung Neoplasms: mortality,Male,Myeloid,Oligonucleotide Array Sequence Analysis,Precursor Cell Lymphoblastic Leukemia-Lymphoma,Precursor Cell Lymphoblastic Leukemia-Lymphoma: ge,Tumor,p53,p53: physiology},
number = {43},
pages = {15545--15550},
pmid = {16199517},
title = {{Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles.}},
volume = {102},
year = {2005}
}
@article{Santarius2010,
abstract = {Integrated genome-wide screens of DNA copy number and gene expression in human cancers have accelerated the rate of discovery of amplified and overexpressed genes. However, the biological importance of most of the genes identified in such studies remains unclear. In this Analysis, we propose a weight-of-evidence based classification system for identifying individual genes in amplified regions that are selected for during tumour development. In a census of the published literature we have identified 77 genes for which there is good evidence of involvement in the development of human cancer.},
author = {Santarius, Thomas and Shipley, Janet and Brewer, Daniel and Stratton, Michael R. and Cooper, Colin S.},
doi = {10.1038/nrc2771},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Santarius et al. - 2010 - A census of amplified and overexpressed human cancer genes.pdf:pdf},
isbn = {1474-1768 (Electronic)$\backslash$r1474-175X (Linking)},
issn = {1474-1768},
journal = {Nat. Rev. Cancer},
keywords = {cancer,genes and mutations,review},
mendeley-tags = {cancer,genes and mutations,review},
number = {1},
pages = {59--64},
pmid = {20029424},
publisher = {Nature Publishing Group},
title = {{A census of amplified and overexpressed human cancer genes.}},
volume = {10},
year = {2010}
}
@article{Gelber2008,
abstract = {Objectives: This study examined associations between anthropometric measures (body mass index, waist circumference, waist-to-hip ratio, waist-to-height ratio [WHtR]) and risk of incident cardiovascular disease (CVD) (including nonfatal myocardial infarction, nonfatal ischemic stroke, and cardiovascular death). Background: Controversy exists regarding the optimal approach to measure adiposity, and the utility of body mass index has been questioned. Methods: Participants included 16,332 men in the Physicians' Health Study (mean age 61 years in 1991) and 32,700 women in the Women's Health Study (mean age 61 years in 1999). We used Cox proportional hazards models to determine relative risks and 95{\%} confidence intervals (CIs) for developing CVD according to self-reported anthropometric indexes. Results: A total of 1,505 CVD cases occurred in men and 414 occurred in women (median follow-up 14.2 and 5.5 years, respectively). Although WHtR demonstrated statistically the strongest associations with CVD and best model fit, CVD risk increased linearly and significantly with higher levels of all indexes. Adjusting for confounders, the relative risk for CVD was 0.58 (95{\%} CI: 0.32 to 1.05) for men with the lowest WHtR ({\textless}0.45) and 2.36 (95{\%} CI: 1.61 to 3.47) for the highest WHtR (???0.69; vs. WHtR 0.49 to {\textless}0.53). Among women, the relative risk was 0.65 (95{\%} CI: 0.33 to 1.31) for those with the lowest WHtR ({\textless}0.42) and 2.33 (95{\%} CI: 1.66 to 3.28) for the highest WHtR (???0.68; vs. WHtR 0.47 to {\textless}0.52). Conclusions: The WHtR demonstrated statistically the best model fit and strongest associations with CVD. However, compared with body mass index, differences in cardiovascular risk assessment using other indexes were small and likely not clinically consequential. Our findings emphasize that higher levels of adiposity, however measured, confer increased risk of CVD. ?? 2008 American College of Cardiology Foundation.},
author = {Gelber, Rebecca P. and Gaziano, J. Michael and Orav, E. John and Manson, JoAnn E. and Buring, Julie E. and Kurth, Tobias},
doi = {10.1016/j.jacc.2008.03.066},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Gelber et al. - 2008 - Measures of Obesity and Cardiovascular Risk Among Men and Women.pdf:pdf},
isbn = {07351097},
issn = {07351097},
journal = {J. Am. Coll. Cardiol.},
keywords = {cardiovascular disease,epidemiology,obesity},
mendeley-tags = {obesity},
number = {8},
pages = {605--615},
pmid = {18702962},
publisher = {Elsevier Masson SAS},
title = {{Measures of Obesity and Cardiovascular Risk Among Men and Women}},
volume = {52},
year = {2008}
}
@misc{GEO,
author = {{National Center for Biotechnology Information}},
title = {{Gene Expression Omnibus}},
url = {https://www.ncbi.nlm.nih.gov/geo/},
urldate = {2015-03-31},
year = {2016}
}
@article{Gandini2008,
abstract = {We conducted a systematic meta-analysis of observational studies on$\backslash$ncigarette smoking and cancer from 1961 to 2003. The aim was to quantify$\backslash$nthe risk for 13 cancer sites, recognized to be related to tobacco$\backslash$nsmoking by the International Agency for Research on Cancer (IARC), and$\backslash$nto analyze the risk variation for each site in a systematic manner. We$\backslash$nextracted data from 254 reports published between 1961 and 2003 (177$\backslash$ncase-control studies, 75 cohorts and 2 nested case-control studies)$\backslash$nincluded in the 2004 IARC Monograph on Tobacco Smoke and Involuntary$\backslash$nSmoking. The analyses were carried out on 216 studies with reported$\backslash$nestimates for `current' and/or `former' smokers. We performed$\backslash$nsensitivity analysis, and looked for publication and other types of$\backslash$nbias. Lung (RR = 8.96; 95{\%} CI: 6.73-12.11), laryngeal (RR = 6.98; 95{\%}$\backslash$nCl: 3.14-15.52) and pharyngeal (RR = 6.76; 95{\%} CI: 2.86-15.98) cancers$\backslash$npresented the highest relative risks (RRs) for current smokers, followed$\backslash$nby upper digestive tract (RR = 3.57; 95{\%} CI: 2.63-4.84) and oral (RR =$\backslash$n3.43; 95{\%} CI: 2.37-4.94) cancers. As expected, pooled RRs for$\backslash$nrespiratory cancers were greater than the pooled estimates for other$\backslash$nsites. The analysis of heterogeneity showed that study type, gender and$\backslash$nadjustment for confounding factors significantly influence the RRs$\backslash$nestimates and the reliability of the studies.},
author = {Gandini, Sara and Botteri, Edoardo and Iodice, Simona and Boniol, Mathieu and Lowenfels, Albert B. and Maisonneuve, Patrick and Boyle, Peter},
doi = {10.1002/ijc.23033},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Gandini et al. - 2008 - Tobacco smoking and cancer A meta-analysis.pdf:pdf},
isbn = {1097-0215 (Electronic)$\backslash$n0020-7136 (Linking)},
issn = {00207136},
journal = {Int. J. Cancer},
keywords = {Cancer,Meta-analysis,Tobacco,environmental factors,lung cancer,tobacco},
mendeley-tags = {environmental factors,lung cancer,tobacco},
number = {1},
pages = {155--164},
pmid = {17893872},
title = {{Tobacco smoking and cancer: A meta-analysis}},
volume = {122},
year = {2008}
}
@misc{Løning2013a,
abstract = {Following their successful implementation for the treatment of metastatic breast cancer, the 'third-generation' aromatase inhibitors (anastrozole, letrozole, and exemestane) have now become standard adjuvant endocrine treatment for postmenopausal estrogen receptor-positive breast cancers. These drugs are characterized by potent aromatase inhibition, causing {\textgreater}98{\%} inhibition of estrogen synthesis in vivo. A recent meta-analysis found no difference in anti-tumor efficacy between these three compounds. As of today, aromatase inhibitor monotherapy and sequential treatment using tamoxifen followed by an aromatase inhibitor for a total of 5 years are considered equipotent treatment options. However, current trials are addressing the potential benefit of extending treatment duration beyond 5 years. Regarding side effects, aromatase inhibitors are not found associated with enhanced risk of cardiovascular disease, and enhanced bone loss is prevented by adding bisphosphonates in concert for those at danger of developing osteoporosis. However, arthralgia and carpal tunnel syndrome preclude drug administration among a few patients. While recent findings have questioned the use of aromatase inhibitors among overweight and, in particular, obese patients, this problem seems to focus on premenopausal patients treated with an aromatase inhibitor and an LH-RH analog in concert, questioning the efficacy of LH-RH analogs rather than aromatase inhibitors among overweight patients. Finally, recent findings revealing a benefit from adding the mTOR inhibitor everolimus to endocrine treatment indicate targeted therapy against defined growth factor pathways to be a way forward, by reversing acquired resistance to endocrine therapy.},
author = {L{\o}ning, Per Eystein and Eikesdal, Hans Petter},
booktitle = {Endocr. Relat. Cancer},
doi = {10.1530/ERC-13-0099},
file = {:Users/rikutakei/Documents/Mendeley Desktop/L{\o}ning, Eikesdal{\_}2013{\_}Aromatase inhibition 2013 Clinical state of the art and questions that remain to be solved.pdf:pdf},
isbn = {1479-6821 (Electronic)$\backslash$n1351-0088 (Linking)},
issn = {13510088},
keywords = {Adjuvant therapy,Aromatase inhibitors,Breast cancer,Endocrine therapy,Resistance},
number = {4},
pmid = {23625614},
title = {{Aromatase inhibition 2013: Clinical state of the art and questions that remain to be solved}},
volume = {20},
year = {2013}
}
@article{WHO2010,
abstract = {In May 2004, the 57th World Health Assembly (WHA) endorsed the World Health Organization (WHO) Global Strategy on Diet, Physical Activity and Health. The Strategy was developed through a wide-ranging series of consultations with all concerned stakeholders in response to a request from Member States at World Health Assembly 2002 (Resolution WHA55.23). The Strategy, together with the Resolution by which it was endorsed (WHA57.17), are contained in this document.},
archivePrefix = {arXiv},
arxivId = {arXiv:gr-qc/9809069v1},
author = {{World Health Organisation}},
doi = {10.1080/11026480410034349},
eprint = {9809069v1},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/World Health Organisation - 2010 - Global recommendations on physical activity for health.pdf:pdf},
isbn = {978 92 4 159 997 9},
issn = {11026480},
journal = {Geneva World Heal. Organ.},
keywords = {obesity},
mendeley-tags = {obesity},
pmid = {20963782},
primaryClass = {arXiv:gr-qc},
title = {{Global recommendations on physical activity for health}},
year = {2010}
}
@article{Wang2007,
abstract = {This review of the obesity epidemic provides a comprehensive description of the current situation, time trends, and disparities across gender, age, socioeconomic status, racial/ethnic groups, and geographic regions in the United States based on national data. The authors searched studies published between 1990 and 2006. Adult overweight and obesity were defined by using body mass index (weight (kg)/height (m)2) cutpoints of 25 and 30, respectively; childhood “at risk for overweight” and overweight were defined as the 85th and 95th percentiles of body mass index. Average annual increase in and future projections for prevalence were estimated by using linear regression models. Among adults, obesity prevalence increased from 13{\%} to 32{\%} between the 1960s and 2004. Currently, 66{\%} of adults are overweight or obese; 16{\%} of children and adolescents are overweight and 34{\%} are at risk of overweight. Minority and low-socioeconomic-status groups are disproportionately affected at all ages. Annual increases in prevalence ranged from 0.3 to 0.9 percentage points across groups. By 2015, 75{\%} of adults will be overweight or obese, and 41{\%} will be obese. In conclusion, obesity has increased at an alarming rate in the United States over the past three decades. The associations of obesity with gender, age, ethnicity, and socioeconomic status are complex and dynamic. Related population-based programs and policies are needed.},
author = {Wang, Youfa and Beydoun, May A.},
doi = {10.1093/epirev/mxm007},
file = {:Users/rikutakei/Downloads/papers/mxm007.pdf:pdf},
isbn = {0193-936X (Print)$\backslash$r0193-936X (Linking)},
issn = {0193936X},
journal = {Epidemiol. Rev.},
keywords = {Body mass index,Ethnic groups,Obesity,Overweight,Social class,United States},
number = {1},
pages = {6--28},
pmid = {17510091},
title = {{The obesity epidemic in the United States - Gender, age, socioeconomic, racial/ethnic, and geographic characteristics: A systematic review and meta-regression analysis}},
volume = {29},
year = {2007}
}
@article{Diepgen2002,
abstract = {Melanoma and non-melanoma (basal and squamous cell carcinoma) skin cancer (NMSC) are now the most common types of cancer in the white populations and the incidence of skin cancer has reached epidemic proportions. According to recent population-based studies from Australia the incidence rate is over 2{\%} for basal cell carcinoma in males and 1{\%} for squamous cell carcinoma, and there are over 50 new cases of melanoma per 100 000.},
author = {Diepgen, T. L. and Mahler, V.},
doi = {10.1046/j.1365-2133.146.s61.2.x},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Diepgen, Mahler - 2002 - Epidemiology of skin cancer.pdf:pdf},
isbn = {1365-2133},
issn = {0172780X},
journal = {Br. J. Dermatol.},
keywords = {Actinic keratoses,Basal cell carcinoma,Bowen's disease,Cutaneous tumors,Epidemiology,Melanoma,Skin cancer,Squamous cell carcinoma,cancer,environmental factors,uv},
mendeley-tags = {cancer,environmental factors,uv},
pages = {1--6},
pmid = {11966724},
title = {{Epidemiology of skin cancer}},
volume = {146},
year = {2002}
}
@article{Sporn1997,
abstract = {25 years ago, then President Nixon 'declared' War on Cancer. In this personal commentary, the war is reviewed. There have been obvious triumphs, for instance in cure of acute lymphocytic leukaemia and other childhood cancers, Hodgkin's disease, and testicular cancer. However, substantial advances in molecular oncology have yet to impinge on mortality statistics. Too many adults still die from common epithelial cancers. Failure to appreciate that local invasion and distant metastasis rather then cell proliferation itself are lethal, obsession with cure of advanced disease rather than prevention of early disease, and neglect of the need to arrest preneoplastic lesions may all have served to make victory elusive.},
author = {Sporn, Michael B.},
doi = {10.1111/j.1749-6632.1997.tb48599.x},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Sporn - 1997 - The war on cancer A review.pdf:pdf},
isbn = {0140-6736 (Print)$\backslash$n0140-6736 (Linking)},
issn = {00778923},
journal = {Ann. N. Y. Acad. Sci.},
keywords = {cancer},
mendeley-tags = {cancer},
number = {1996},
pages = {137--146},
pmid = {9616746},
title = {{The war on cancer: A review}},
volume = {833},
year = {1997}
}
@article{Dixon2016,
abstract = {BACKGROUND Observational studies have reported a positive association between body mass index (BMI) and ovarian cancer risk. However, questions remain as to whether this represents a causal effect, or holds for all histological subtypes. The lack of association observed for serous cancers may, for instance, be due to disease-associated weight loss. Mendelian randomization (MR) uses genetic markers as proxies for risk factors to overcome limitations of observational studies. We used MR to elucidate the relationship between BMI and ovarian cancer, hypothesizing that genetically predicted BMI would be associated with increased risk of non-high grade serous ovarian cancers (non-HGSC) but not HGSC. METHODS We pooled data from 39 studies (14 047 cases, 23 003 controls) in the Ovarian Cancer Association Consortium. We constructed a weighted genetic risk score (GRS, partial F-statistic = 172), summing alleles at 87 single nucleotide polymorphisms previously associated with BMI, weighting by their published strength of association with BMI. Applying two-stage predictor-substitution MR, we used logistic regression to estimate study-specific odds ratios (OR) and 95{\%} confidence intervals (CI) for the association between genetically predicted BMI and risk, and pooled these using random-effects meta-analysis. RESULTS Higher genetically predicted BMI was associated with increased risk of non-HGSC (pooled OR = 1.29, 95{\%} CI 1.03-1.61 per 5 units BMI) but not HGSC (pooled OR = 1.06, 95{\%} CI 0.88-1.27). Secondary analyses stratified by behaviour/subtype suggested that, consistent with observational data, the association was strongest for low-grade/borderline serous cancers (OR = 1.93, 95{\%} CI 1.33-2.81). CONCLUSIONS Our data suggest that higher BMI increases risk of non-HGSC, but not the more common and aggressive HGSC subtype, confirming the observational evidence.},
author = {Dixon, Suzanne C and Nagle, Christina M and Thrift, Aaron P and Pharoah, Paul D P and Pearce, Celeste Leigh and Zheng, Wei and Painter, Jodie N and Chenevix-Trench, Aocs Group Australian Cancer Study Ovarian Cancer Georgia and Fasching, Peter A and Beckmann, Matthias W and Lambrechts, Diether and Vergote, Ignace and Lambrechts, Sandrina and {Van Nieuwenhuysen}, Els and Rossing, Mary Anne and Doherty, Jennifer A and Wicklund, Kristine G and Chang-Claude, Jenny and Rudolph, Anja and Moysich, Kirsten B and Odunsi, Kunle and Goodman, Marc T and Wilkens, Lynne R and Thompson, Pamela J and Shvetsov, Yurii B and D{\"{o}}rk, Thilo and Park-Simon, Tjoung-Won and Hillemanns, Peter and Bogdanova, Natalia and Butzow, Ralf and Nevanlinna, Heli and Pelttari, Liisa M and Leminen, Arto and Modugno, Francesmary and Ness, Roberta B and Edwards, Robert P and Kelley, Joseph L and Heitz, Florian and Karlan, Beth Y and Kj{\ae}r, Susanne K and H{\o}gdall, Estrid and Jensen, Allan and Goode, Ellen L and Fridley, Brooke L and Cunningham, Julie M and Winham, Stacey J and Giles, Graham G and Bruinsma, Fiona and Milne, Roger L and Southey, Melissa C and Hildebrandt, Michelle A T and Wu, Xifeng and Lu, Karen H and Liang, Dong and Levine, Douglas A and Bisogna, Maria and Schildkraut, Joellen M and Berchuck, Andrew and Cramer, Daniel W and Terry, Kathryn L and Bandera, Elisa V and Olson, Sara H and Salvesen, Helga B and Thomsen, Liv Cecilie and Kopperud, Reidun K and Bjorge, Line and Kiemeney, Lambertus A and Massuger, Leon F A G and Pejovic, Tanja and Cook, Linda S and Le, Nhu D and Swenerton, Kenneth D and Brooks-Wilson, Angela and Kelemen, Linda E and Lubi{\'{n}}ski, Jan and Huzarski, Tomasz and Gronwald, Jacek and Menkiszak, Janusz and Wentzensen, Nicolas and Brinton, Louise and Yang, Hannah and Lissowska, Jolanta and H{\o}gdall, Claus K and Lundvall, Lene and Song, Honglin and Tyrer, Jonathan P and Campbell, Ian and Eccles, Diana and Paul, James and Glasspool, Rosalind and Siddiqui, Nadeem and Whittemore, Alice S and Sieh, Weiva and McGuire, Valerie and Rothstein, Joseph H and Narod, Steven A and Phelan, Catherine and Risch, Harvey A and McLaughlin, John R and Anton-Culver, Hoda and Ziogas, Argyrios and Menon, Usha and Gayther, Simon A and Ramus, Susan J and Gentry-Maharaj, Aleksandra and Wu, Anna H and Pike, Malcolm C and Tseng, Chiu-Chen and Kupryjanczyk, Jolanta and Dansonka-Mieszkowska, Agnieszka and Budzilowska, Agnieszka and Spiewankiewicz, Beata and Webb, Penelope M and {Ovarian Cancer Association Consortium}},
doi = {10.1093/ije/dyw158},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Dixon et al. - 2016 - Adult body mass index and risk of ovarian cancer by subtype a Mendelian randomization study.pdf:pdf},
issn = {1464-3685},
journal = {Int. J. Epidemiol.},
keywords = {Body mass index,Mendelian randomization analysis,obesity,ovarian neoplasms},
pages = {1--12},
pmid = {27401727},
title = {{Adult body mass index and risk of ovarian cancer by subtype: a Mendelian randomization study.}},
year = {2016}
}
@article{Kanehisa2000,
author = {Kanehisa, Minoru and Goto, Susumu},
doi = {10.1093/nar/27.1.29},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Kanehisa, Goto - 2000 - KEGG Kyoto encyclopedia of genes and genomes.pdf:pdf},
isbn = {0305-1048 (Print)$\backslash$r0305-1048 (Linking)},
issn = {03051048},
journal = {Nucleic Acids Res.},
number = {1},
pages = {27--30},
pmid = {10592173},
title = {{KEGG: Kyoto encyclopedia of genes and genomes}},
volume = {28},
year = {2000}
}
@article{Yach2006,
abstract = {Conclusion: The absence of definitive evidence of strategies that will work to reduce overweight and obesity should not delay action. When several Nordic countries as well as Canada, New Zealand and Singapore pioneered comprehensive tobacco control in the early 1970s, they relied on sound economic and consumer theory. Over time, their intuition that smokers would respond to price, marketing, access to treatment and ever- expanding education programs, has proven correct. Adapting these basic principles to the much more complex areas of food, nutri- tion and physical activity will be tougher and will require broader alliances between public, private and civil societies. The consequences of inaction-reversal of steady improvements in life expectancy, and rising costs should be sufficient motivation for urgent action.},
archivePrefix = {arXiv},
arxivId = {arXiv:1011.1669v3},
author = {Yach, Derek and Stuckler, David and Brownell, Kelly D},
doi = {10.1038/nm0306-367a},
eprint = {arXiv:1011.1669v3},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Yach, Stuckler, Brownell - 2006 - Epidemiologic and economic consequences of the global epidemics of obesity and diabetes.pdf:pdf},
isbn = {1078-8956 (Print)$\backslash$r1078-8956 (Linking)},
issn = {1078-8956},
journal = {Nat. Med.},
keywords = {obesity risk},
mendeley-tags = {obesity risk},
number = {1},
pages = {62--66},
pmid = {16397571},
title = {{Epidemiologic and economic consequences of the global epidemics of obesity and diabetes.}},
volume = {12},
year = {2006}
}
@article{Bruning2000,
abstract = {Insulin receptors (IRs) and insulin signaling proteins are widely distributed throughout the central nervous system (CNS). To study the physiological role of insulin signaling in the brain, we created mice with a neuron-specific disruption of the IR gene (NIRKO mice). Inactivation of the IR had no impact on brain development or neuronal survival. However, female NIRKO mice showed increased food intake, and both male and female mice developed diet-sensitive obesity with increases in body fat and plasma leptin levels, mild insulin resistance, elevated plasma insulin levels, and hypertriglyceridemia. NIRKO mice also exhibited impaired spermatogenesis and ovarian follicle maturation because of hypothalamic dysregulation of luteinizing hormone. Thus, IR signaling in the CNS plays an important role in regulation of energy disposal, fuel metabolism, and reproduction.},
author = {Br{\"{u}}ning, Jens C and Gautam, Dinesh and Burks, Deborah J and Gillette, Jennifer and Schubert, Markus and Orban, Paul C and Klein, R{\"{u}}diger and Krone, Wilhelm and M{\"{u}}ller-Wieland, Dirk and Kahn, C Ronald},
doi = {10.1126/science.289.5487.2122},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Br{\"{u}}ning et al. - 2000 - Role of Brain Insulin Receptor in Control of Body Weight and Reproduction.pdf:pdf},
isbn = {0036-8075},
issn = {0036-8075},
journal = {Science (80-. ).},
keywords = {insulin},
mendeley-tags = {insulin},
number = {5487},
pages = {2122--2125},
title = {{Role of Brain Insulin Receptor in Control of Body Weight and Reproduction}},
volume = {289},
year = {2000}
}
@article{Fridman2003,
abstract = {The p53 tumor suppressor acts to integrate multiple stress signals into a series of diverse antiproliferative responses. One of the most important p53 functions is its ability to activate apoptosis, and disruption of this process can promote tumor progression and chemoresistance. p53 apparently promotes apoptosis through transcription-dependent and -independent mechanisms that act in concert to ensure that the cell death program proceeds efficiently. Moreover, the apoptotic activity of p53 is tightly controlled, and is influenced by a series of quantitative and qualitative events that influence the outcome of p53 activation. Interestingly, other p53 family members can also promote apoptosis, either in parallel or in concert with p53. Although incomplete, our current understanding of p53 illustrates how apoptosis can be integrated into a larger tumor suppressor network controlled by different signals, environmental factors, and cell type. Understanding this network in more detail will provide insights into cancer and other diseases, and will identify strategies to improve their therapeutic treatment.},
author = {Fridman, Jordan S and Lowe, Scott W},
doi = {10.1038/sj.onc.1207116},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Fridman, Lowe - 2003 - Control of apoptosis by p53.pdf:pdf},
isbn = {0950-9232},
issn = {0950-9232},
journal = {Oncogene},
keywords = {and behavior of cells,apoptosis,cancer,hussain and,in a,maintain tissue homeostasis,organism,p53,p63,p73,particular tissue within an,that is,to control the number,tumor suppressor,tumor suppressors act to},
mendeley-tags = {cancer,p53},
number = {56},
pages = {9030--9040},
pmid = {14663481},
title = {{Control of apoptosis by p53}},
volume = {22},
year = {2003}
}
@article{Cairns2011,
abstract = {Interest in the topic of tumour metabolism has waxed and waned over the past century of cancer research. The early observations of Warburg and his contemporaries established that there are fundamental differences in the central metabolic pathways operating in malignant tissue. However, the initial hypotheses that were based on these observations proved inadequate to explain tumorigenesis, and the oncogene revolution pushed tumour metabolism to the margins of cancer research. In recent years, interest has been renewed as it has become clear that many of the signalling pathways that are affected by genetic mutations and the tumour microenvironment have a profound effect on core metabolism, making this topic once again one of the most intense areas of research in cancer biology.},
author = {Cairns, RA and Harris, IS and Mak, TW},
doi = {10.1038/nrc2981},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Cairns, Harris, Mak - 2011 - Regulation of cancer cell metabolism.pdf:pdf},
isbn = {1474-1768 (Electronic)$\backslash$r1474-175X (Linking)},
issn = {1474-1768},
journal = {Nat. Rev. Cancer},
keywords = {Cell Transformation: Neoplastic,Gene Expression Regulation: Neoplastic,Gene Regulatory Networks,Humans,Intracellular Signaling Peptides and Proteins,Neoplasms,Oxidation-Reduction,Signal Transduction,Transcription Factors,cancer,energy},
mendeley-tags = {cancer,energy},
number = {2},
pages = {85--95},
pmid = {21258394},
publisher = {Nature Publishing Group},
title = {{Regulation of cancer cell metabolism}},
volume = {11},
year = {2011}
}
@article{Garofalo2006,
abstract = {The prevalence of obesity has markedly increased over the past two decades, especially in the industrialized countries. While the impact of excess body weight on the development of cardiac disease and diabetes has been well documented, the link between obesity and carcinogenesis is just being recognized. This review will focus on the link between leptin, a cytokine that is elevated in obese individuals, and cancer development. First, we briefly discuss the biological functions of leptin and its signaling pathways. Then, we summarize the effects of leptin on different cancer types in experimental cellular and animal models. Next, we analyze epidemiological data on the relationship between obesity and the presence of cancer or cancer risk in patients. Finally, leptin as a target for cancer treatment and prevention will be discussed.},
archivePrefix = {arXiv},
arxivId = {NIHMS150003},
author = {Garofalo, Cecilia and Surmacz, Eva},
doi = {10.1002/JCP},
eprint = {NIHMS150003},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Garofalo, Surmacz - 2006 - Leptin and Cancer.pdf:pdf},
isbn = {0021-9541},
issn = {0021-9541},
journal = {J. Cell. Physiol.},
keywords = {Animals,Cell Proliferation/drug effects,Humans,Leptin/blood/pharmacology/physiology,Metabolism/drug effects,Neoplasms/blood/physiopathology,Obesity/blood/physiopathology,Risk Factors,Signal Transduction/physiology,cancer,leptin},
mendeley-tags = {cancer,leptin},
number = {1},
pages = {12--22},
pmid = {451},
title = {{Leptin and Cancer}},
volume = {207},
year = {2006}
}
@article{Seoane2003,
abstract = {Ghrelin, the endogenous ligand of the GH secretagogue receptor, acts at central level to elicit GH release and regulate food intake. To elucidate the neural circuit that exerts its effects, we measured the expression of hypothalamic neuropeptides involved in weight regulation and GH secretion after ghrelin administration. Adult male rats, fed or fasted for 72 h, were treated centrally (intracerebroventicularly) with a single dose of ghrelin (5 micro g). After 2, 4, and 6 or 8 h, agouti-related peptide, melanin-concentrating hormone, neuropeptide Y, prepro-orexin, GHRH, and somatostatin mRNA levels were measured by in situ hybridization. We found that ghrelin increased agouti-related peptide and neuropeptide Y expression in the arcuate nucleus of the hypothalamus of fed and fasted rats. In contrast, no change was demonstrated in the mRNA levels of the other neuropeptides studied at any time evaluated. Finally, we examined the effect of ghrelin on GHRH and somatostatin mRNA levels in GH-deficient (dwarf) rats. Our results show that ghrelin increases somatostatin mRNA levels in the hypothalamus of these rats. This study furthers our understanding of the molecular basis and mechanisms involved in the effect of ghrelin on food intake and GH secretion.},
author = {Seoane, Luisa M. and L{\'{o}}pez, Miguel and Tovar, Sulay and Casanueva, Felipe F. and Se{\~{n}}ar{\'{i}}s, Rosa and Di{\'{e}}guez, Carlos},
doi = {10.1210/en.2002-220795},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Seoane et al. - 2003 - Agouti-related peptide, neuropeptide Y, and somatostatin-producing neurons are targets for ghrelin actions in the.pdf:pdf},
isbn = {0013-7227 (Print)$\backslash$r0013-7227 (Linking)},
issn = {00137227},
journal = {Endocrinology},
number = {2},
pages = {544--551},
pmid = {12538615},
title = {{Agouti-related peptide, neuropeptide Y, and somatostatin-producing neurons are targets for ghrelin actions in the rat hypothalamus}},
volume = {144},
year = {2003}
}
@article{Sacks2009,
abstract = {A comprehensive policy approach is needed to control the growing obesity epidemic. This paper proposes the Obesity Policy Action (OPA) framework, modified from the World Health Organization framework for the implementation of the Global Strategy on Diet, Physical Activity and Health, to provide specific guidance for governments to systematically identify areas for obesity policy action. The proposed framework incorporates three different public health approaches to addressing obesity: (i) 'upstream' policies influence either the broad social and economic conditions of society (e.g. taxation, education, social security) or the food and physical activity environments to make healthy eating and physical activity choices easier; (ii) 'midstream' policies are aimed at directly influencing population behaviours; and (iii) 'downstream' policies support health services and clinical interventions. A set of grids for analysing potential policies to support obesity prevention and management is presented. The general pattern that emerges from populating the analysis grids as they relate to the Australian context is that all sectors and levels of government, non-governmental organizations and private businesses have multiple opportunities to contribute to reducing obesity. The proposed framework and analysis grids provide a comprehensive approach to mapping the policy environment related to obesity, and a tool for identifying policy gaps, barriers and opportunities.},
author = {Sacks, G. and Swinburn, B. and Lawrence, M.},
doi = {10.1111/j.1467-789X.2008.00524.x},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Sacks, Swinburn, Lawrence - 2009 - Obesity Policy Action framework and analysis grids for a comprehensive policy approach to reducing ob.pdf:pdf},
isbn = {1467-789X},
issn = {14677881},
journal = {Obes. Rev.},
keywords = {Framework,Obesity prevention,Policy,obesity},
mendeley-tags = {obesity},
number = {1},
pages = {76--86},
pmid = {18761640},
title = {{Obesity Policy Action framework and analysis grids for a comprehensive policy approach to reducing obesity}},
volume = {10},
year = {2009}
}
@article{Suzuki2004,
abstract = {Aberrant WNT pathway signaling is an early progression event in 90{\%} of colorectal cancers. It occurs through mutations mainly of APC and less often of CTNNB1 (encoding beta-catenin) or AXIN2 (encoding axin-2, also known as conductin). These mutations allow ligand-independent WNT signaling that culminates in abnormal accumulation of free beta-catenin in the nucleus. We previously identified frequent promoter hypermethylation and gene silencing of the genes encoding secreted frizzled-related proteins (SFRPs) in colorectal cancer. SFRPs possess a domain similar to one in the WNT-receptor frizzled proteins and can inhibit WNT receptor binding to downregulate pathway signaling during development. Here we show that restoration of SFRP function in colorectal cancer cells attenuates WNT signaling even in the presence of downstream mutations. We also show that the epigenetic loss of SFRP function occurs early in colorectal cancer progression and may thus provide constitutive WNT signaling that is required to complement downstream mutations in the evolution of colorectal cancer.},
author = {Suzuki, Hiromu and Watkins, D Neil and Jair, Kam-Wing and Schuebel, Kornel E and Markowitz, Sanford D and Chen, Wei Dong and Pretlow, Theresa P and Yang, Bin and Akiyama, Yoshimitsu and {Van Engeland}, Manon and Toyota, Minoru and Tokino, Takashi and Hinoda, Yuji and Imai, Kohzoh and Herman, James G and Baylin, Stephen B},
doi = {10.1038/ng1330},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Suzuki et al. - 2004 - Epigenetic inactivation of SFRP genes allows constitutive WNT signaling in colorectal cancer.pdf:pdf},
isbn = {1061-4036 (Print)$\backslash$n1061-4036 (Linking)},
issn = {1061-4036},
journal = {Nat. Genet.},
keywords = {Cell Line,Colorectal Neoplasms,Colorectal Neoplasms: genetics,Colorectal Neoplasms: metabolism,Colorectal Neoplasms: pathology,Gene Silencing,Glycoproteins,Glycoproteins: metabolism,Humans,Proto-Oncogene Proteins,Proto-Oncogene Proteins: metabolism,Reverse Transcriptase Polymerase Chain Reaction,Signal Transduction,Tumor,Wnt Proteins,cancer},
mendeley-tags = {cancer},
number = {4},
pages = {417--422},
pmid = {15034581},
title = {{Epigenetic inactivation of SFRP genes allows constitutive WNT signaling in colorectal cancer.}},
volume = {36},
year = {2004}
}
@article{Must1999,
abstract = {This report reviews the risks and consequences associated with childhood and adolescent obesity. Although no consensus definition of childhood obesity exists, the various measures encountered in the literature are moderately well correlated. The paper is organized in three parts. The first section reviews childhood obesity sequelae that occur during childhood. These short-term risks, for orthopedic, neurological, pulmonary, gasteroenterological, and endocrine conditions, although largely limited to severely overweight children, are becoming more common as the prevalence of severe overweight rises. The social burden of pediatric obesity, especially during middle childhood and adolescence, may have lasting effects on self-esteem, body image and economic mobility. The second section examines the intermediate consequences, such as the development of cardiovascular risk factors and persistence of obesity into adulthood. These mid-range effects of early obesity presage later adult disease and premature mortality. In the final section, the small body of research on the long-term morbidity and mortality associated with childhood obesity is reviewed. These studies suggest that risk of cardiovascular disease and all-cause mortality is elevated among those who were overweight during childhood. The high prevalence and dramatic secular trend toward increasing childhood obesity suggest that without aggressive approaches to prevention and treatment, the attendant health and social consequences will be both substantial and long-lasting.},
author = {Must, A and Strauss, R S},
doi = {10.1038/sj/ijo/0800852},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Must, Strauss - 1999 - Risks and consequences of childhood and adolescent obesity.pdf:pdf},
isbn = {0307-0565 (Print)},
issn = {0307-0565},
journal = {Int. J. Obes. Relat. Metab. Disord.},
keywords = {adolescent obesity,childhood obesity,morbidity,obesity risk,persistence,risk factors},
mendeley-tags = {obesity risk},
pages = {S2--S11},
pmid = {10340798},
title = {{Risks and consequences of childhood and adolescent obesity.}},
volume = {23},
year = {1999}
}
@article{Soon2011,
abstract = {Secretory factors that drive cancer progression are attractive immunotherapeutic targets. We used a whole-genome data-mining approach on multiple cohorts of breast tumours annotated for clinical outcomes to discover such factors. We identified Serine protease inhibitor Kazal-type 1 (SPINK1) to be associated with poor survival in estrogen receptor-positive (ER+) cases. Immunohistochemistry showed that SPINK1 was absent in normal breast, present in early and advanced tumours, and its expression correlated with poor survival in ER+ tumours. In ER- cases, the prognostic effect did not reach statistical significance. Forced expression and/or exposure to recombinant SPINK1 induced invasiveness without affecting cell proliferation. However, down-regulation of SPINK1 resulted in cell death. Further, SPINK1 overexpressing cells were resistant to drug-induced apoptosis due to reduced caspase-3 levels and high expression of Bcl2 and phospho-Bcl2 proteins. Intriguingly, these anti-apoptotic effects of SPINK1 were abrogated by mutations of its protease inhibition domain. Thus, SPINK1 affects multiple aggressive properties in breast cancer: survival, invasiveness and chemoresistance. Because SPINK1 effects are abrogated by neutralizing antibodies, we suggest that SPINK1 is a viable potential therapeutic target in breast cancer.},
author = {Soon, Wendy Weijia and Miller, Lance David and Black, Michael A. and Dalmasso, Cyril and Chan, Xiu Bin and Pang, Brendan and Ong, Chee Wee and Salto-Tellez, Manuel and Desai, Kartiki V. and Liu, Edison T.},
doi = {10.1002/emmm.201100150},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Soon et al.{\_}2011{\_}Combined genomic and phenotype screening reveals secretory factor SPINK1 as an invasion and survival factor associated.pdf:pdf},
isbn = {1757-4684 (Electronic)$\backslash$r1757-4676 (Linking)},
issn = {17574676},
journal = {EMBO Mol. Med.},
keywords = {Breast cancer,Cancer therapy,Distant metastasis-free survival,Expression microarrays,Oncogenes},
pages = {451--464},
pmid = {21656687},
title = {{Combined genomic and phenotype screening reveals secretory factor SPINK1 as an invasion and survival factor associated with patient prognosis in breast cancer}},
volume = {3},
year = {2011}
}
@article{Coller2000,
abstract = {MYC affects normal and neoplastic cell proliferation by altering gene expression, but the precise pathways remain unclear. We used oligonucleotide microarray analysis of 6,416 genes and expressed sequence tags to determine changes in gene expression caused by activation of c-MYC in primary human fibroblasts. In these experiments, 27 genes were consistently induced, and 9 genes were repressed. The identity of the genes revealed that MYC may affect many aspects of cell physiology altered in transformed cells: cell growth, cell cycle, adhesion, and cytoskeletal organization. Identified targets possibly linked to MYC's effects on cell growth include the nucleolar proteins nucleolin and fibrillarin, as well as the eukaryotic initiation factor 5A. Among the cell cycle genes identified as targets, the G1 cyclin D2 and the cyclin-dependent kinase binding protein CksHs2 were induced whereas the cyclin-dependent kinase inhibitor p21(Cip1) was repressed. A role for MYC in regulating cell adhesion and structure is suggested by repression of genes encoding the extracellular matrix proteins fibronectin and collagen, and the cytoskeletal protein tropomyosin. A possible mechanism for MYC-mediated apoptosis was revealed by identification of the tumor necrosis factor receptor associated protein TRAP1 as a MYC target. Finally, two immunophilins, peptidyl-prolyl cis-trans isomerase F and FKBP52, the latter of which plays a role in cell division in Arabidopsis, were up-regulated by MYC. We also explored pattern-matching methods as an alternative approach for identifying MYC target genes. The genes that displayed an expression profile most similar to endogenous Myc in microarray-based expression profiling of myeloid differentiation models were highly enriched for MYC target genes.},
archivePrefix = {arXiv},
arxivId = {nature.vol.342.30nov1989},
author = {Coller, H A and Grandori, C and Tamayo, P and Colbert, T and Lander, E S and Eisenman, R N and Golub, T R},
doi = {10.1073/pnas.97.7.3260},
eprint = {nature.vol.342.30nov1989},
file = {:Users/rikutakei/Downloads/papers/PNAS-2000-Coller-3260-5.pdf:pdf},
isbn = {0027-8424 (Print)$\backslash$r0027-8424 (Linking)},
issn = {0027-8424},
journal = {Proc. Natl. Acad. Sci. U. S. A.},
keywords = {Blotting,Cell Adhesion,Cell Adhesion: genetics,Cell Cycle,Cell Cycle: genetics,Cell Differentiation,Cell Differentiation: genetics,Cell Division,Cell Division: genetics,Cell Line,Gene Expression Regulation,Gene Expression Regulation: physiology,Genetic Vectors,Humans,Northern,Oligonucleotides,Oligonucleotides: chemistry,Proto-Oncogene Proteins c-myc,Proto-Oncogene Proteins c-myc: physiology,Signal Transduction,Signal Transduction: genetics},
number = {7},
pages = {3260--3265},
pmid = {10737792},
title = {{Expression analysis with oligonucleotide microarrays reveals that MYC regulates genes involved in growth, cell cycle, signaling, and adhesion.}},
volume = {97},
year = {2000}
}
@misc{Carlson2016,
author = {Carlson, M},
title = {{GO.db: A set of annotation maps describing the entire Gene Ontology. R package version 3.4.0}},
year = {2016}
}
@book{Health2016,
address = {Wellington},
author = {{New Zealand Ministry of Health}},
file = {:Users/rikutakei/Downloads/papers/annual-update-key-results-2015-16-nzhs-dec16-v2.pdf:pdf},
isbn = {9780478444650},
keywords = {2013/14 NZHS,NZHS,New Zealand Health Survey,hea},
pages = {1--87},
publisher = {Ministry of Health},
title = {{Annual Update of Key Results 2015/16: New Zealand Health Survey.}},
year = {2016}
}
@article{Spiegelman2001,
abstract = {Obesity is defined medically as a state of increased body weight, more specifically adipose tissue, of sufficient magnitude to produce adverse health consequences. There has been an alarming increase recently in the prevalence of this heterogeneous group of disorders in the Western world (Kuczmarski et al., 1994). Fully one- third of the American population is now considered obese, and the prevalence of obesity in children is esca- lating dramatically, presaging even greater medical harm in the decades to come (Troiano and Flegal, 1999). What accounts for this epidemic of energy storage? Bodyweight and composition, andthe storage of energy as triglyceride in adipose tissue, are determined by the interaction between genetic, environmental, and psy- chosocial factors. These influences ultimately act by changing the energy balance equation, that is, the long- term balance between energy intake and expenditure. Physiologic studies had previously suggested that body weight and energy stores are homeostatically regulated, with either weight loss or gain producing concerted changes in energy intake and expenditure that resist the initial perturbation. Recent cloning of several obesity genes has revealed the initial molecular components of a coherent physiologic system for energy homeostasis (Barsh et al., 2000). Studies of obesity pathogenesis must now attempt to explain the disorder in the context of this physiologic system.},
author = {Spiegelman, Bruce M. and Flier, Jeffrey S.},
doi = {10.1016/S0092-8674(01)00240-9},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Spiegelman, Flier - 2001 - Obesity and the regulation of energy balance.pdf:pdf},
isbn = {0092-8674},
issn = {00928674},
journal = {Cell},
keywords = {obesity},
mendeley-tags = {obesity},
number = {4},
pages = {531--543},
pmid = {11239410},
title = {{Obesity and the regulation of energy balance}},
volume = {104},
year = {2001}
}
@article{Ollmann1997,
abstract = {Expression of Agouti protein is normally limited to the skin where it affects pigmentation, but ubiquitous expression causes obesity. An expressed sequence tag was identified that encodes Agouti-related protein, whose RNA is normally expressed in the hypothalamus and whose levels were increased eightfold in ob/ob mice. Recombinant Agouti-related protein was a potent, selective antagonist of Mc3r and Mc4r, melanocortin receptor subtypes implicated in weight regulation. Ubiquitous expression of human AGRP complementary DNA in transgenic mice caused obesity without altering pigmentation. Thus, Agouti-related protein is a neuropeptide implicated in the normal control of body weight downstream of leptin signaling.},
author = {Ollmann, M M and Wilson, B D and Yang, Y K and Kerns, J A and Chen, Y and Gantz, I and Barsh, G S},
doi = {10.1126/science.278.5335.135},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Ollmann et al. - 1997 - Antagonism of central melanocortin receptors in vitro and in vivo by agouti-related protein.pdf:pdf},
isbn = {0036-8075 (Print)$\backslash$r0036-8075 (Linking)},
issn = {00368075},
journal = {Science (80-. ).},
keywords = {obesity},
mendeley-tags = {obesity},
number = {5335},
pages = {135--138},
pmid = {9311920},
title = {{Antagonism of central melanocortin receptors in vitro and in vivo by agouti-related protein}},
volume = {278},
year = {1997}
}
@article{Samatar2014,
abstract = {The RAS-RAF-MEK-ERK signalling pathway is hyperactivated in a high percentage of tumours, most frequently owing to activating mutations of the KRAS, NRAS and BRAF genes. Recently, the use of compounds targeting components of ERK signalling, such as RAF or MEK inhibitors, has led to substantial improvement in clinical outcome in metastatic melanoma and has shown promising clinical activity in additional tumour types. However, response rates are highly variable and the efficacy of these drugs is primarily limited by the development of resistance. Both intrinsic and acquired resistance to RAF and MEK inhibitors are frequently associated with the persistence of ERK signalling in the presence of the drug, implying the need for more innovative approaches to target the pathway.},
author = {Samatar, Ahmed a. and Poulikakos, Poulikos I.},
doi = {10.1038/nrd4281},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Samatar, Poulikakos - 2014 - Targeting RAS–ERK signalling in cancer promises and challenges.pdf:pdf},
isbn = {1474-1784 (Electronic)$\backslash$n1474-1776 (Linking)},
issn = {1474-1776},
journal = {Nat. Rev. Drug Discov.},
keywords = {Animals,Antineoplastic Agents,Antineoplastic Agents: administration {\&} dosage,Drug Delivery Systems,Drug Delivery Systems: trends,Humans,MAP Kinase Signaling System,MAP Kinase Signaling System: drug effects,MAP Kinase Signaling System: physiology,Neoplasms,Neoplasms: drug therapy,Neoplasms: metabolism,Protein Kinase Inhibitors,Protein Kinase Inhibitors: administration {\&} dosage,Ras,cancer,ras Proteins,ras Proteins: antagonists {\&} inhibitors,ras Proteins: metabolism},
mendeley-tags = {Ras,cancer},
number = {12},
pages = {928--942},
pmid = {25435214},
publisher = {Nature Publishing Group},
title = {{Targeting RAS–ERK signalling in cancer: promises and challenges}},
volume = {13},
year = {2014}
}
@article{Hanahan2000,
author = {Hanahan, Douglas and Weinberg, Robert A.},
doi = {10.1016/S0092-8674(00)81683-9},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Hanahan, Weinberg{\_}2000{\_}The hallmarks of cancer.pdf:pdf},
isbn = {0026201009680},
issn = {00928674},
journal = {Cell},
keywords = {Key Paper},
mendeley-tags = {Key Paper},
pages = {57--70},
pmid = {19636327},
title = {{The hallmarks of cancer}},
volume = {100},
year = {2000}
}
@article{Leek2012,
abstract = {Heterogeneity and latent variables are now widely recognized as major sources of bias and variability in high-throughput experiments. The most well-known source of latent variation in genomic experiments are batch effects-when samples are processed on different days, in different groups or by different people. However, there are also a large number of other variables that may have a major impact on high-throughput measurements. Here we describe the sva package for identifying, estimating and removing unwanted sources of variation in high-throughput experiments. The sva package supports surrogate variable estimation with the sva function, direct adjustment for known batch effects with the ComBat function and adjustment for batch and latent variables in prediction problems with the fsva function.},
author = {Leek, Jeffrey T. and Johnson, W. Evan and Parker, Hilary S. and Jaffe, Andrew E. and Storey, John D.},
doi = {10.1093/bioinformatics/bts034},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Leek et al. - 2012 - The SVA package for removing batch effects and other unwanted variation in high-throughput experiments.pdf:pdf},
isbn = {1367480314602059},
issn = {13674803},
journal = {Bioinformatics},
number = {6},
pages = {882--883},
pmid = {22257669},
title = {{The SVA package for removing batch effects and other unwanted variation in high-throughput experiments}},
volume = {28},
year = {2012}
}
@article{Dubern2001,
abstract = {OBJECTIVE: To search for mutations in melanocortin pathway elements, that is, the melanocortin-4 receptor (MC4R), agouti-related protein (AGRP), and alpha-melanocyte-stimulating hormone (alpha MSH) genes in children with severe obesity. STUDY DESIGN: Direct sequencing of the MC4R encoding sequence and single-strand polymorphism conformation analysis of AGRP and alpha MSH genes were performed in 63 severely obese children. Polymerase chain reaction (PCR) assays of restriction fragment length polymorphism were used to assess the frequency of each newly discovered mutation in 283 non-obese control subjects. RESULTS: Four dominantly inherited, heterozygous, missense MC4R mutations (Val50Met, Ser58Cys, Ile102Ser, and Ile170Val) were identified in 4 unrelated children and none of the control subjects. Expression of the obese phenotype was variable in mutation-positive family members. Clinical and laboratory features were similar in the obese children with and without an MC4R mutation. Two polymorphisms were detected in the AGRP -encoding sequence (a silent mutation in exon 1 and Ala67Thr in exon 2), with similar frequencies in the obese and control groups. No mutations were found in the alpha MSH gene. CONCLUSIONS: MC4R mutations may be a non-negligible cause of severe obesity in children with variable expression and penetrance. Mutations in AGRP and alpha MSH genes were not among the causes of obesity in our population.},
author = {Dubern, B and Cl{\'{e}}ment, K and Pelloux, V and Froguel, P and Girardet, J P and Guy-Grand, B and Tounian, P},
doi = {10.1067/mpd.2001.116284},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Dubern et al. - 2001 - Mutational analysis of melanocortin-4 receptor, agouti-related protein, and alpha-melanocyte-stimulating hormone.pdf:pdf},
isbn = {0022-3476},
issn = {0022-3476},
journal = {J. Pediatr.},
keywords = {obesity},
mendeley-tags = {obesity},
number = {2},
pages = {204--209},
pmid = {11487744},
title = {{Mutational analysis of melanocortin-4 receptor, agouti-related protein, and alpha-melanocyte-stimulating hormone genes in severely obese children.}},
volume = {139},
year = {2001}
}
@article{Malik2013,
abstract = {The worldwide increase in obesity and related chronic diseases has largely been driven by global trade liberalization, economic growth and rapid urbanization. These factors continue to fuel dramatic changes in living environments, diets and lifestyles in ways that promote positive energy balance. Nutritional transitions in low-income and middle-income countries are typically characterized by increases in the consumption of animal fat and protein, refined grains, and added sugar. This change is coupled with reductions in physical activity owing to more mechanized and technologically driven lifestyles. Given the high costs of obesity and comorbidities in terms of health-care expenditure and quality of life, prevention strategies are paramount, particularly in low-income and middle-income countries that must manage coexisting infectious diseases and undernutrition in addition to the obesity epidemic. As countries become increasingly urbanized, undernutrition and obesity can exist side by side within the same country, community or household, which is a particular challenge for health systems with limited resources. Owing to the scope and complexity of the obesity epidemic, prevention strategies and policies across multiple levels are needed in order to have a measurable effect. Changes should include high-level global policies from the international community and coordinated efforts by governments, organizations, communities and individuals to positively influence behavioural change.},
author = {Malik, Vasanti S and Willett, Walter C and Hu, Frank B},
doi = {10.1038/nrendo.2012.199},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Malik, Willett, Hu - 2013 - Global obesity trends, risk factors and policy implications.pdf:pdf},
isbn = {1759-5029},
issn = {1759-5037},
journal = {Nat. Rev. Endocrinol.},
keywords = {Health Promotion,Humans,Life Style,Obesity,Obesity: epidemiology,Risk Factors,World Health,obesity},
mendeley-tags = {obesity},
number = {1},
pages = {13--27},
pmid = {23165161},
publisher = {Nature Publishing Group},
title = {{Global obesity: trends, risk factors and policy implications.}},
volume = {9},
year = {2013}
}
@article{Shimizu2012a,
abstract = {PURPOSE: This study evaluated the clinical relevance of the dual-targeting strategy involving PI3K/AKT/mTOR and RAF/MEK/ERK pathways. EXPERIMENTAL DESIGN: We investigated safety, efficacy, and correlations between tumor genetic alterations and clinical benefit in 236 patients with advanced cancers treated with phase I study drugs targeting phosphoinositide 3-kinase (PI3K) and/or mitogen-activated protein kinase (MAPK) pathways in our Phase I Clinical Trials Program. RESULTS: Seventy-six (32.2{\%}) patients received a PI3K pathway inhibitor in combination with a MAPK pathway inhibitor (D), whereas 124 (52.5{\%}) and 36 (15.3{\%}), respectively, received an inhibitor of either the PI3K or MAPK pathways (S). The rates of drug-related grade {\textgreater}III adverse events were 18.1{\%} for (S) and 53.9{\%} for (D; P {\textless} 0.001); the rates of dose-limiting toxicities were 9.4{\%} for (S) and 18.4{\%} for (D; P = 0.06). The most frequent grade {\textgreater}III adverse events were transaminase elevations, skin rash, and mucositis. In our comprehensive tumor genomic analysis, of 9 patients who harbored coactivation of both pathways (colorectal cancer, n = 7; melanoma, n = 2), all 5 patients treated with (D) had tumor regression ranging from 2{\%} to 64{\%}. CONCLUSIONS: These results suggest that dual inhibition of both pathways may potentially exhibit favorable efficacy compared with inhibition of either pathway, at the expense of greater toxicity. Furthermore, this parallel pathway targeting strategy may be especially important in patients with coexisting PI3K pathway genetic alterations and KRAS or BRAF mutations and suggests that molecular profiling and matching patients with combinations of these targeted drugs will need to be investigated in depth.},
author = {Shimizu, Toshio and Tolcher, Anthony W. and Papadopoulos, Kyriakos P. and Beeram, Muralidhar and Rasco, Drew W. and Smith, Lon S. and Gunn, Shelly and Smetzer, Leslie and Mays, Theresa A. and Kaiser, Brianne and Wick, Michael J. and Alvarez, Cathy and Cavazos, Aracely and Mangold, Gina L. and Patnaik, Amita},
doi = {10.1158/1078-0432.CCR-11-2381},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Shimizu et al. - 2012 - The clinical effect of the dual-targeting strategy involving PI3KAKTmTOR and RASMEKERK pathways in patients with.pdf:pdf},
isbn = {1078-0432 (Print)$\backslash$r1078-0432 (Linking)},
issn = {10780432},
journal = {Clin. Cancer Res.},
keywords = {cancer,combinatorial therapy},
mendeley-tags = {cancer,combinatorial therapy},
number = {8},
pages = {2316--2325},
pmid = {22261800},
title = {{The clinical effect of the dual-targeting strategy involving PI3K/AKT/mTOR and RAS/MEK/ERK pathways in patients with advanced cancer}},
volume = {18},
year = {2012}
}
@article{Kanehisa2008,
abstract = {KEGG (http://www.genome.jp/kegg/) is a database of biological systems that integrates genomic, chemical and systemic functional information. KEGG provides a reference knowledge base for linking genomes to life through the process of PATHWAY mapping, which is to map, for example, a genomic or transcriptomic content of genes to KEGG reference pathways to infer systemic behaviors of the cell or the organism. In addition, KEGG provides a reference knowledge base for linking genomes to the environment, such as for the analysis of drug-target relationships, through the process of BRITE mapping. KEGG BRITE is an ontology database representing functional hierarchies of various biological objects, including molecules, cells, organisms, diseases and drugs, as well as relationships among them. KEGG PATHWAY is now supplemented with a new global map of metabolic pathways, which is essentially a combined map of about 120 existing pathway maps. In addition, smaller pathway modules are defined and stored in KEGG MODULE that also contains other functional units and complexes. The KEGG resource is being expanded to suit the needs for practical applications. KEGG DRUG contains all approved drugs in the US and Japan, and KEGG DISEASE is a new database linking disease genes, pathways, drugs and diagnostic markers.},
author = {Kanehisa, Minoru and Araki, Michihiro and Goto, Susumu and Hattori, Masahiro and Hirakawa, Mika and Itoh, Masumi and Katayama, Toshiaki and Kawashima, Shuichi and Okuda, Shujiro and Tokimatsu, Toshiaki and Yamanishi, Yoshihiro},
doi = {10.1093/nar/gkm882},
file = {:Users/rikutakei/Downloads/papers/gkm882.pdf:pdf},
isbn = {1362-4962 (Electronic)$\backslash$r0305-1048 (Linking)},
issn = {03051048},
journal = {Nucleic Acids Res.},
number = {SUPPL. 1},
pages = {480--484},
pmid = {18077471},
title = {{KEGG for linking genomes to life and the environment}},
volume = {36},
year = {2008}
}
@article{Dawood2008,
abstract = {PURPOSE: The purpose of this retrospective study was to determine the association and prognostic value of body mass index (BMI) at the time of initial diagnosis in patients with locally advanced breast cancer (LABC). The analysis includes the subsets of inflammatory (IBC) and noninflammatory (non-IBC LABC) breast cancer. EXPERIMENTAL DESIGN: We identified 602 patients who had LABC treated on prospective clinical trials. BMI was divided into three groups: (a) {\textless} or =24.9 (normal/underweight), (b) 25.0 to 29.9 (overweight), and (c) {\textgreater} or =30 (obese). Kaplan-Meier product limit method was used to estimate survival outcomes. Cox proportional hazards were used to determine associations between survival and BMI and to test for an interaction between BMI and breast cancer type. RESULTS: Eighty-two percent had non-IBC LABC and 18{\%} had IBC. Obese patients tended to have a higher incidence of IBC compared with overweight and normal/underweight groups (P = 0.01). Median follow up was 6 years for all patients. Median overall survival (OS) and recurrence-free survival (RFS) were 8.8 and 5.9 years, respectively. Patients with LABC who were obese or overweight had a significantly worse OS and RFS (P = 0.001) and a higher incidence of visceral recurrence compared with normal/underweight patients. In a multivariable model, BMI remained significantly associated with both OS and RFS for the entire cohort. The interactions between BMI and LABC subsets and between BMI and menopausal status were not statistically significant. CONCLUSION: Patients with LABC and high BMI have a worse prognosis. Evaluation of the biological factors associated with this observation can provide tools for additional therapeutic interventions.},
author = {Dawood, Shaheenah and Broglio, Kristine and Gonzalez-Angulo, Ana M and Kau, Shu-Wan and Islam, Rabiul and Hortobagyi, Gabriel N and Cristofanilli, Massimo},
doi = {10.1158/1078-0432.CCR-07-1479},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Dawood et al.{\_}2008{\_}Prognostic value of body mass index in locally advanced breast cancer.pdf:pdf},
issn = {1078-0432},
journal = {Clin. Cancer Res.},
number = {6},
pages = {1718--1725},
pmid = {18347172},
title = {{Prognostic value of body mass index in locally advanced breast cancer.}},
volume = {14},
year = {2008}
}
@article{Tarca2013,
abstract = {Identification of functional sets of genes associated with conditions of interest from omics data was first reported in 1999, and since, a plethora of enrichment methods were published for systematic analysis of gene sets collections including Gene Ontology and biological pathways. Despite their widespread usage in reducing the complexity of omics experiment results, their performance is poorly understood. Leveraging the existence of disease specific gene sets in KEGG and Metacore{\textregistered} databases, we compared the performance of sixteen methods under relaxed assumptions while using 42 real datasets (over 1,400 samples). Most of the methods ranked high the gene sets designed for specific diseases whenever samples from affected individuals were compared against controls via microarrays. The top methods for gene set prioritization were different from the top ones in terms of sensitivity, and four of the sixteen methods had large false positives rates assessed by permuting the phenotype of the samples. The best overall methods among those that generated reasonably low false positive rates, when permuting phenotypes, were PLAGE, GLOBALTEST, and PADOG. The best method in the category that generated higher than expected false positives was MRGSE.},
author = {Tarca, Adi L. and Bhatti, Gaurav and Romero, Roberto},
doi = {10.1371/journal.pone.0079217},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Tarca, Bhatti, Romero - 2013 - A comparison of gene set analysis methods in terms of sensitivity, prioritization and specificity.pdf:pdf},
isbn = {1932-6203},
issn = {19326203},
journal = {PLoS One},
number = {11},
pages = {e79217},
pmid = {24260172},
title = {{A comparison of gene set analysis methods in terms of sensitivity, prioritization and specificity}},
volume = {8},
year = {2013}
}
@article{Lahav2004,
abstract = {The tumor suppressor p53, one of the most intensely investigated proteins, is usually studied by experiments that are averaged over cell populations, potentially masking the dynamic behavior in individual cells. We present a system for following, in individual living cells, the dynamics of p53 and its negative regulator Mdm2 (refs. 1,4-7): this system uses functional p53-CFP and Mdm2-YFP fusion proteins and time-lapse fluorescence microscopy. We found that p53 was expressed in a series of discrete pulses after DNA damage. Genetically identical cells had different numbers of pulses: zero, one, two or more. The mean height and duration of each pulse were fixed and did not depend on the amount of DNA damage. The mean number of pulses, however, increased with DNA damage. This approach can be used to study other signaling systems and suggests that the p53-Mdm2 feedback loop generates a 'digital' clock that releases well-timed quanta of p53 until damage is repaired or the cell dies.},
author = {Lahav, Galit and Rosenfeld, Nitzan and Sigal, Alex and Geva-Zatorsky, Naama and Levine, Arnold J and Elowitz, Michael B and Alon, Uri},
doi = {10.1038/ng1293},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Lahav et al. - 2004 - Dynamics of the p53-Mdm2 feedback loop in individual cells.pdf:pdf},
isbn = {1061-4036 (Print)$\backslash$r1061-4036 (Linking)},
issn = {1061-4036},
journal = {Nat. Genet.},
keywords = {mdm2,p53},
mendeley-tags = {mdm2,p53},
number = {2},
pages = {147--150},
pmid = {14730303},
title = {{Dynamics of the p53-Mdm2 feedback loop in individual cells.}},
volume = {36},
year = {2004}
}
@article{Neel1962,
abstract = {FOR THE POPULATION GENETICIST, diabetes mellitus has long presented an enigma. Here is a relatively frequent disease, often interfering with reproduction by virtue of an onset during the reproductive or even pre-reproductive years, with a well-defined genetic basis, perhaps as simple in many families as a single recessive or incompletely recessive gene (cf. Allan, 1933; Pincus and White, 1933, 1934; Harris, 1950; Steinberg and Wilder, 1952; Lamy, Frezal and de Grouchy, 1957; Steinberg, 1959; Post, 1962a). If the considerable frequency of the disease is of relatively long duration in the history of our species, how can this be accounted for in the face of the obvious and strong genetic selection against the condition? If, on the other hand, this frequency is a relatively recent phenomenon, what changes in the environment are responsible for the increase? Current developments in the study of this disease suggest an explanation with important biological ramifications.},
author = {Neel, J. V.},
doi = {10.1007/SpringerReference_98337},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Neel - 1962 - Diabetes mellitus a thrifty genotype rendered detrimental by progress 1962.pdf:pdf},
isbn = {0002929700029297},
issn = {00429686},
journal = {Am. J. Hum. Genet.},
keywords = {obesity},
mendeley-tags = {obesity},
number = {4},
pages = {353--362},
pmid = {13937884},
title = {{Diabetes mellitus: a "thrifty" genotype rendered detrimental by "progress"? 1962.}},
volume = {14},
year = {1962}
}
@article{Lichtenstein2000,
author = {Lichtenstein, Paul and Holm, Niels V. and Verkasalo, Pia K. and Iliadou, Anastasia and Kaprio, Jaako and Koskenvuo, Markku and Pukkala, Eero and Skytthe, Axel and Hemminki, Kari},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Lichtenstein et al. - 2000 - Environmental and heritable factors in the causation of cancer Analyses of cohorts of twins from Sweden, De.pdf:pdf},
journal = {N. Engl. J. Med.},
keywords = {cancer,environmental factors},
mendeley-tags = {cancer,environmental factors},
number = {2},
pages = {78--85},
title = {{Environmental and heritable factors in the causation of cancer: Analyses of cohorts of twins from Sweden, Denmark, and Finland}},
volume = {343},
year = {2000}
}
@article{Kazerounian2008,
abstract = {Abstract.  Thrombospondin-1 is a secreted protein that modulates vascular cell behavior via several cell surface receptors. In vitro, nanomolar concentrations of thrombospondin-1 are required to alter endothelial and vascular smooth muscle cell adhesion, proliferation, motility, and survival. Yet, much lower levels of thrombospondin-1 are clearly functional in vivo. This discrepancy was explained with the discovery that the potency of thrombospondin-1 increases more than 100-fold in the presence of physiological levels of nitric oxide (NO). Thrombospondin-1 binding to CD47 inhibits NO signaling by preventing cGMP synthesis and activation of its target cGMP-dependent protein kinase. This potent antagonism of NO signaling allows thrombospondin-1 to acutely constrict blood vessels, accelerate platelet aggregation, and if sustained, inhibit angiogenic responses. Acute antagonism of NO signaling by thrombospondin-1 is important for hemostasis but becomes detrimental for tissue survival of ischemic injuries. New therapeutic approaches targeting thrombospondin-1 or CD47 can improve recovery from ischemic injuries and overcome a deficit in NO-responsiveness in aging. (Part of a Multi-author Review)},
author = {Kazerounian, S. and Yee, K. O. and Lawler, J.},
doi = {10.1007/s00018-007-7486-z},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Kazerounian, Yee, Lawler - 2008 - Thrombospondins From structure to therapeutics - Thrombospondins in cancer.pdf:pdf},
isbn = {1420-682X},
issn = {1420682X},
journal = {Cell. Mol. Life Sci.},
keywords = {Angiogenesis,Cancer,TSP1,Thrombospondin,Transforming growth factor ??,Tumor dormancy,angiogenesis,cancer},
mendeley-tags = {TSP1,angiogenesis,cancer},
number = {5},
pages = {700--712},
pmid = {18193165},
title = {{Thrombospondins: From structure to therapeutics - Thrombospondins in cancer}},
volume = {65},
year = {2008}
}
@article{Tomasetti2015,
author = {Tomasetti, Cristian and Vogelstein, Bert},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Tomasetti, Vogelstein - 2015 - Cancer risk Role of environment Cancer risk Tumors excluded Cancer risk Role of chance overstated Canc.pdf:pdf},
journal = {Science (80-. ).},
keywords = {cancer,environmental factors},
mendeley-tags = {cancer,environmental factors},
number = {160},
pages = {730--731},
title = {{Cancer risk : Role of environment Cancer risk : Tumors excluded Cancer risk : Role of chance overstated Cancer risk : Prevention is crucial Cancer risk : Many factors contribute}},
volume = {347},
year = {2015}
}
@article{Cully2006,
abstract = {The tumour-suppressor phosphatase with tensin homology (PTEN) is the most important negative regulator of the cell-survival signalling pathway initiated by phosphatidylinositol 3-kinase (PI3K). Although PTEN is mutated or deleted in many tumours, deregulation of the PI3K-PTEN network also occurs through other mechanisms. Crosstalk between the PI3K pathways and other tumorigenic signalling pathways, such as those that involve Ras, p53, TOR (target of rapamycin) or DJ1, can contribute to this deregulation. How does the PI3K pathway integrate signals from numerous sources, and how can this information be used in the rational design of cancer therapies?},
author = {Cully, M and You, H and Levine, A J and Mak, T W},
doi = {10.1038/nrc1819},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Cully et al. - 2006 - Beyond PTEN mutations the PI3K pathway as an integrator of multiple inputs during tumorigenesis.pdf:pdf},
isbn = {1474-175X (Print)$\backslash$r1474-175X (Linking)},
issn = {1474-175X},
journal = {Nat. Rev. Cancer},
keywords = {Animals,Cell Transformation,Humans,Mutation/*genetics,Neoplasms/*enzymology/genetics,Neoplastic,PI3K,PTEN Phosphohydrolase/*genetics/metabolism,Phosphatidylinositol 3-Kinases/*metabolism,Signal Transduction,Tumor Suppressor Proteins,cancer},
mendeley-tags = {PI3K,cancer},
number = {3},
pages = {184--192},
pmid = {16453012},
title = {{Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis}},
volume = {6},
year = {2006}
}
@article{Yusuf2005,
abstract = {BACKGROUND: Obesity is a major risk factor for cardiovascular disease, but the most predictive measure for different ethnic populations is not clear. We aimed to assess whether markers of obesity, especially waist-to-hip ratio, would be stronger indicators of myocardial infarction than body-mass index (BMI), the conventional measure. METHODS: We did a standardised case-control study of acute myocardial infarction with 27 098 participants in 52 countries (12,461 cases and 14,637 controls) representing several major ethnic groups. We assessed the relation between BMI, waist and hip circumferences, and waist-to-hip ratio to myocardial infarction overall and for each group. FINDINGS: BMI showed a modest and graded association with myocardial infarction (OR 1.44, 95{\%} CI 1.32-1.57 top quintile vs bottom quintile before adjustment), which was substantially reduced after adjustment for waist-to-hip ratio (1.12, 1.03-1.22), and non-significant after adjustment for other risk factors (0.98, 0.88-1.09). For waist-to-hip ratio, the odds ratios for every successive quintile were significantly greater than that of the previous one (2nd quintile: 1.15, 1.05-1.26; 3rd quintile: 1.39; 1.28-1.52; 4th quintile: 1.90, 1.74-2.07; and 5th quintiles: 2.52, 2.31-2.74 [adjusted for age, sex, region, and smoking]). Waist (adjusted OR 1.77; 1.59-1.97) and hip (0.73; 0.66-0.80) circumferences were both highly significant after adjustment for BMI (p{\textless}0.0001 top vs bottom quintiles). Waist-to-hip ratio and waist and hip circumferences were closely (p{\textless}0.0001) associated with risk of myocardial infarction even after adjustment for other risk factors (ORs for top quintile vs lowest quintiles were 1.75, 1.33, and 0.76, respectively). The population-attributable risks of myocardial infarction for increased waist-to-hip ratio in the top two quintiles was 24.3{\%} (95{\%} CI 22.5-26.2) compared with only 7.7{\%} (6.0-10.0) for the top two quintiles of BMI. INTERPRETATION: Waist-to-hip ratio shows a graded and highly significant association with myocardial infarction risk worldwide. Redefinition of obesity based on waist-to-hip ratio instead of BMI increases the estimate of myocardial infarction attributable to obesity in most ethnic groups.},
author = {Yusuf, Salim and Hawken, Steven and Ounpuu, Stephanie and Bautista, Leonelo and Franzosi, Maria Grazia and Commerford, Patrick and Lang, Chim C and Rumboldt, Zvonko and Onen, Churchill L and Lisheng, Liu and Tanomsup, Supachai and Wangai, Paul and Razak, Fahad and Sharma, Arya M and Anand, Sonia S},
doi = {10.1016/S0140-6736(05)67663-5},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Yusuf et al. - 2005 - Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries a case-control study.pdf:pdf},
isbn = {1474-547X},
issn = {1474-547X},
journal = {Lancet},
keywords = {obesity},
mendeley-tags = {obesity},
number = {9497},
pages = {1640--1649},
pmid = {16271645},
title = {{Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study.}},
volume = {366},
year = {2005}
}
@article{Renehan2008,
abstract = {BACKGROUND: Excess bodyweight, expressed as increased body-mass index (BMI), is associated with the risk of some common adult cancers. We did a systematic review and meta-analysis to assess the strength of associations between BMI and different sites of cancer and to investigate differences in these associations between sex and ethnic groups.$\backslash$n$\backslash$nMETHODS: We did electronic searches on Medline and Embase (1966 to November 2007), and searched reports to identify prospective studies of incident cases of 20 cancer types. We did random-effects meta-analyses and meta-regressions of study-specific incremental estimates to determine the risk of cancer associated with a 5 kg/m2 increase in BMI.$\backslash$n$\backslash$nFINDINGS: We analysed 221 datasets (141 articles), including 282,137 incident cases. In men, a 5 kg/m2 increase in BMI was strongly associated with oesophageal adenocarcinoma (RR 1.52, p{\textless}0.0001) and with thyroid (1.33, p=0.02), colon (1.24, p{\textless}0.0001), and renal (1.24, p {\textless}0.0001) cancers. In women, we recorded strong associations between a 5 kg/m2 increase in BMI and endometrial (1.59, p{\textless}0.0001), gallbladder (1.59, p=0.04), oesophageal adenocarcinoma (1.51, p{\textless}0.0001), and renal (1.34, p{\textless}0.0001) cancers. We noted weaker positive associations (RR {\textless}1.20) between increased BMI and rectal cancer and malignant melanoma in men; postmenopausal breast, pancreatic, thyroid, and colon cancers in women; and leukaemia, multiple myeloma, and non-Hodgkin lymphoma in both sexes. Associations were stronger in men than in women for colon (p{\textless}0.0001) cancer. Associations were generally similar in studies from North America, Europe and Australia, and the Asia-Pacific region, but we recorded stronger associations in Asia-Pacific populations between increased BMI and premenopausal (p=0.009) and postmenopausal (p=0.06) breast cancers.$\backslash$n$\backslash$nINTERPRETATION: Increased BMI is associated with increased risk of common and less common malignancies. For some cancer types, associations differ between sexes and populations of different ethnic origins. These epidemiological observations should inform the exploration of biological mechanisms that link obesity with cancer.},
author = {Renehan, Andrew G and Tyson, Margaret and Egger, Matthias and Heller, Richard F and Zwahlen, Marcel},
doi = {10.1016/S0140-6736(08)60269-X},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Renehan et al. - 2008 - Body-mass index and incidence of cancer a systematic review and meta-analysis of prospective observational studi.pdf:pdf},
isbn = {1474-547X (Electronic) 0140-6736 (Linking)},
issn = {1474-547X},
journal = {Lancet},
keywords = {Body Mass Index,Ethnic Groups,Female,Humans,Male,Neoplasms,Neoplasms: etiology,Overweight,Overweight: complications,Regression Analysis,Risk,Sex Factors,obesity and cancer},
mendeley-tags = {obesity and cancer},
number = {November},
pages = {569--78},
pmid = {18280327},
title = {{Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies.}},
volume = {371},
year = {2008}
}
@article{Bild2009,
abstract = {INTRODUCTION: Perhaps the major challenge in developing more effective therapeutic strategies for the treatment of breast cancer patients is confronting the heterogeneity of the disease, recognizing that breast cancer is not one disease but multiple disorders with distinct underlying mechanisms. Gene-expression profiling studies have been used to dissect this complexity, and our previous studies identified a series of intrinsic subtypes of breast cancer that define distinct populations of patients with respect to survival. Additional work has also used signatures of oncogenic pathway deregulation to dissect breast cancer heterogeneity as well as to suggest therapeutic opportunities linked to pathway activation. METHODS: We used genomic analyses to identify relations between breast cancer subtypes, pathway deregulation, and drug sensitivity. For these studies, we use three independent breast cancer gene-expression data sets to measure an individual tumor phenotype. Correlation between pathway status and subtype are examined and linked to predictions for response to conventional chemotherapies. RESULTS: We reveal patterns of pathway activation characteristic of each molecular breast cancer subtype, including within the more aggressive subtypes in which novel therapeutic opportunities are critically needed. Whereas some oncogenic pathways have high correlations to breast cancer subtype (RAS, CTNNB1, p53, HER1), others have high variability of activity within a specific subtype (MYC, E2F3, SRC), reflecting biology independent of common clinical factors. Additionally, we combined these analyses with predictions of sensitivity to commonly used cytotoxic chemotherapies to provide additional opportunities for therapeutics specific to the intrinsic subtype that might be better aligned with the characteristics of the individual patient. CONCLUSIONS: Genomic analyses can be used to dissect the heterogeneity of breast cancer. We use an integrated analysis of breast cancer that combines independent methods of genomic analyses to highlight the complexity of signaling pathways underlying different breast cancer phenotypes and to identify optimal therapeutic opportunities.},
author = {Bild, A H and Parker, J S and Gustafson, A M and Acharya, C R and Hoadley, K A and Anders, C and Marcom, P K and Carey, L A and Potti, A and Nevins, J R and Perou, C M},
doi = {10.1186/bcr2344},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Bild et al. - 2009 - An integration of complementary strategies for gene-expression analysis to reveal novel therapeutic opportunities f.pdf:pdf},
isbn = {1465-542X (Electronic)$\backslash$r1465-5411 (Linking)},
issn = {1465-542X},
journal = {Breast cancer Res.},
keywords = {*Genetic Heterogeneity,*Oligonucleotide Array Sequence Analysis,Antineoplastic Agents/pharmacology/therapeutic use,Biological/biosynthesis/*genetics,Breast Neoplasms/classification/drug therapy/*gene,Cytotoxins/pharmacology/therapeutic use,Databases,Drug Resistance,Factual,Female,Gene Expression Profiling/*methods,Gene Expression Regulation,Gene Regulatory Networks/genetics,Humans,Metabolic Networks and Pathways/genetics,Neoplasm Proteins/biosynthesis/*genetics,Neoplasm/genetics,Neoplastic,Oncogenes,Phenotype,Signal Transduction/genetics,Tumor Markers},
number = {4},
pages = {R55},
pmid = {19638211},
title = {{An integration of complementary strategies for gene-expression analysis to reveal novel therapeutic opportunities for breast cancer}},
volume = {11},
year = {2009}
}
@article{Løning2013,
abstract = {Following their successful implementation for the treatment of metastatic breast cancer, the 'third-generation' aromatase inhibitors (anastrozole, letrozole, and exemestane) have now become standard adjuvant endocrine treatment for postmenopausal estrogen receptor-positive breast cancers. These drugs are characterized by potent aromatase inhibition, causing {\textgreater}98{\%} inhibition of estrogen synthesis in vivo. A recent meta-analysis found no difference in anti-tumor efficacy between these three compounds. As of today, aromatase inhibitor monotherapy and sequential treatment using tamoxifen followed by an aromatase inhibitor for a total of 5 years are considered equipotent treatment options. However, current trials are addressing the potential benefit of extending treatment duration beyond 5 years. Regarding side effects, aromatase inhibitors are not found associated with enhanced risk of cardiovascular disease, and enhanced bone loss is prevented by adding bisphosphonates in concert for those at danger of developing osteoporosis. However, arthralgia and carpal tunnel syndrome preclude drug administration among a few patients. While recent findings have questioned the use of aromatase inhibitors among overweight and, in particular, obese patients, this problem seems to focus on premenopausal patients treated with an aromatase inhibitor and an LH-RH analog in concert, questioning the efficacy of LH-RH analogs rather than aromatase inhibitors among overweight patients. Finally, recent findings revealing a benefit from adding the mTOR inhibitor everolimus to endocrine treatment indicate targeted therapy against defined growth factor pathways to be a way forward, by reversing acquired resistance to endocrine therapy.},
author = {L{\o}ning, Per Eystein and Eikesdal, Hans Petter},
doi = {10.1530/ERC-13-0099},
file = {:Users/rikutakei/Documents/Mendeley Desktop/L{\o}ning, Eikesdal{\_}2013{\_}Aromatase inhibition 2013 Clinical state of the art and questions that remain to be solved.pdf:pdf},
isbn = {1479-6821 (Electronic)$\backslash$n1351-0088 (Linking)},
issn = {13510088},
journal = {Endocr. Relat. Cancer},
keywords = {Adjuvant therapy,Aromatase inhibitors,Breast cancer,Endocrine therapy,Resistance},
pmid = {23625614},
title = {{Aromatase inhibition 2013: Clinical state of the art and questions that remain to be solved}},
volume = {20},
year = {2013}
}
@article{Yu2009,
abstract = {Commensurate with their roles in regulating cytokine-dependent inflammation and immunity, signal transducer and activator of transcription (STAT) proteins are central in determining whether immune responses in the tumour microenvironment promote or inhibit cancer. Persistently activated STAT3 and, to some extent, STAT5 increase tumour cell proliferation, survival and invasion while suppressing anti-tumour immunity. The persistent activation of STAT3 also mediates tumour-promoting inflammation. STAT3 has this dual role in tumour inflammation and immunity by promoting pro-oncogenic inflammatory pathways, including nuclear factor-kappaB (NF-kappaB) and interleukin-6 (IL-6)-GP130-Janus kinase (JAK) pathways, and by opposing STAT1- and NF-kappaB-mediated T helper 1 anti-tumour immune responses. Consequently, STAT3 is a promising target to redirect inflammation for cancer therapy.},
archivePrefix = {arXiv},
arxivId = {15334406},
author = {Yu, Hua and Pardoll, Drew and Jove, Richard},
doi = {10.1038/nrc2734},
eprint = {15334406},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Yu, Pardoll, Jove - 2009 - STATs in cancer inflammation and immunity a leading role for STAT3.pdf:pdf},
isbn = {1474-1768 (Electronic)$\backslash$r1474-175X (Linking)},
issn = {1474-1768},
journal = {Nat. Rev. Cancer},
keywords = {Animals,Humans,Immunity,Neoplasms,Neoplasms: genetics,Neoplasms: immunology,STAT Transcription Factors,STAT Transcription Factors: genetics,STAT Transcription Factors: immunology,STAT3 Transcription Factor,STAT3 Transcription Factor: genetics,STAT3 Transcription Factor: immunology,STAT5 Transcription Factor,STAT5 Transcription Factor: genetics,STAT5 Transcription Factor: immunology,Signal Transduction,cancer,stat3},
mendeley-tags = {cancer,stat3},
number = {11},
pages = {798--809},
pmid = {19851315},
publisher = {Nature Publishing Group},
title = {{STATs in cancer inflammation and immunity: a leading role for STAT3}},
volume = {9},
year = {2009}
}
@article{Bray2013,
abstract = {Recent estimates of global cancer incidence and survival were used to update previous figures of limited duration prevalence to the year 2008. The number of patients with cancer diagnosed between 2004 and 2008 who were still alive at the end of 2008 in the adult population is described by world region, country and the human development index. The 5-year global cancer prevalence is estimated to be 28.8 million in 2008. Close to half of the prevalence burden is in areas of very high human development that comprise only one-sixth of the world's population. Breast cancer continues to be the most prevalent cancer in the vast majority of countries globally; cervix cancer is the most prevalent cancer in much of Sub-Saharan Africa and Southern Asia and prostate cancer dominates in North America, Oceania and Northern and Western Europe. Stomach cancer is the most prevalent cancer in Eastern Asia (including China); oral cancer ranks as the most prevalent cancer in Indian men and Kaposi sarcoma has the highest 5-year prevalence among men in 11 countries in Sub-Saharan Africa. The methods used to estimate point prevalence appears to give reasonable results at the global level. The figures highlight the need for long-term care targeted at managing patients with certain very frequently diagnosed cancer forms. To be of greater relevance to cancer planning, the estimation of other time-based measures of global prevalence is warranted.},
archivePrefix = {arXiv},
arxivId = {NIHMS150003},
author = {Bray, Freddie and Ren, Jian Song and Masuyer, Eric and Ferlay, Jacques},
doi = {10.1002/ijc.27711},
eprint = {NIHMS150003},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Bray et al. - 2013 - Global estimates of cancer prevalence for 27 sites in the adult population in 2008.pdf:pdf},
isbn = {1097-0215 (Electronic)$\backslash$r0020-7136 (Linking)},
issn = {00207136},
journal = {Int. J. Cancer},
keywords = {cancer facts,development,healthcare facilities,neoplasms,prevalence,survival},
mendeley-tags = {cancer facts},
number = {5},
pages = {1133--1145},
pmid = {22752881},
title = {{Global estimates of cancer prevalence for 27 sites in the adult population in 2008}},
volume = {132},
year = {2013}
}
@article{Gerken2007,
abstract = {Variants in the FTO (fat mass and obesity associated) gene are associated with increased body mass index in humans. Here, we show by bioinformatics analysis that FTO shares sequence motifs with Fe(II)- and 2-oxoglutarate-dependent oxygenases. We find that recombinant murine Fto catalyzes the Fe(II)- and 2OG-dependent demethylation of 3-methylthymine in single-stranded DNA, with concomitant production of succinate, formaldehyde, and carbon dioxide. Consistent with a potential role in nucleic acid demethylation, Fto localizes to the nucleus in transfected cells. Studies of wild-type mice indicate that Fto messenger RNA (mRNA) is most abundant in the brain, particularly in hypothalamic nuclei governing energy balance, and that Fto mRNA levels in the arcuate nucleus are regulated by feeding and fasting. Studies can now be directed toward determining the physiologically relevant FTO substrate and how nucleic acid methylation status is linked to increased fat mass.},
author = {Gerken, Thomas and Girard, Christophe A and Tung, Yi-Chun Loraine and Webby, Celia J and Saudek, Vladimir and Hewitson, Kirsty S and Yeo, Giles S H and McDonough, Michael A and Cunliffe, Sharon and McNeill, Luke A and Galvanovskis, Juris and Rorsman, Patrik and Robins, Peter and Prieur, Xavier and Coll, Anthony P and Ma, Marcella and Jovanovic, Zorica and Farooqi, I Sadaf and Sedgwick, Barbara and Barroso, In{\^{e}}s and Lindahl, Tomas and Ponting, Chris P and Ashcroft, Frances M and O'Rahilly, Stephen and Schofield, Christopher J},
doi = {10.1126/science.1151710},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Gerken et al. - 2007 - The obesity-associated FTO gene encodes a 2-oxoglutarate-dependent nucleic acid demethylase.pdf:pdf},
isbn = {1095-9203 (Electronic)},
issn = {1095-9203},
journal = {Science (80-. ).},
keywords = {FTO,GWAS,obesity},
mendeley-tags = {FTO,GWAS,obesity},
number = {5855},
pages = {1469--1472},
pmid = {17991826},
title = {{The obesity-associated FTO gene encodes a 2-oxoglutarate-dependent nucleic acid demethylase.}},
volume = {318},
year = {2007}
}
@article{Coussens2002,
abstract = {Recent data have expanded the concept that inflammation is a critical component of tumour progression. Many cancers arise from sites of infection, chronic irritation and inflammation. It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration. In addition, tumour cells have co-opted some of the signalling molecules of the innate immune system, such as selectins, chemokines and their receptors for invasion, migration and metastasis. These insights are fostering new anti-inflammatory therapeutic approaches to cancer development.},
author = {Coussens, Lisa M. and Werb, Zena},
doi = {10.1038/nature01322},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Coussens, Werb - 2002 - Inflammation and cancer.pdf:pdf},
isbn = {0028-0836 (Print)$\backslash$r0028-0836 (Linking)},
issn = {0028-0836},
journal = {Nature},
keywords = {cancer,inflammation},
mendeley-tags = {cancer,inflammation},
number = {6917},
pages = {860--867},
pmid = {12490959},
title = {{Inflammation and cancer}},
volume = {420},
year = {2002}
}
@article{Brooks2003,
abstract = {The p53 tumor suppressor exerts anti-proliferative effects, including growth arrest, apoptosis and cell senescence, in response to various types of stress. Tight regulation of p53 activation is imperative for preventing tumorigenesis and maintaining normal cell growth; p53 stabilization and transcriptional activation are crucial early events in a cell's battle against genotoxic stress. Ubiquitination, phosphorylation and acetylation are post-translational modifications to p53 that affect its overall appearance and activity. Recent findings suggest that these modifications have a profound affect on p53 stability and function. Defining the precise roles of these modifications in p53 function may show not only that they are markers of the stress response but also that they serve as the focal point in the regulation of p53.},
author = {Brooks, Christopher L. and Gu, Wei},
doi = {10.1016/S0955-0674(03)00003-6},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Brooks, Gu - 2003 - Ubiquitination, phosphorylation and acetylation The molecular basis for p53 regulation.pdf:pdf},
isbn = {0955-0674 (Print)$\backslash$r0955-0674 (Linking)},
issn = {09550674},
journal = {Curr. Opin. Cell Biol.},
keywords = {cancer,mdm2,p53},
mendeley-tags = {cancer,mdm2,p53},
number = {2},
pages = {164--171},
pmid = {12648672},
title = {{Ubiquitination, phosphorylation and acetylation: The molecular basis for p53 regulation}},
volume = {15},
year = {2003}
}
@article{Wright1989,
abstract = {IMR-90 normal human diploid fibroblasts, transfected with a steroid inducible mouse mammary tumor virus-driven simian virus 40 T antigen, were carried through crisis to yield an immortal cell line. Growth was dependent on the presence of the inducer (dexamethasone) during both the extended precrisis life span of the cells and after immortalization. After dexamethasone removal, immortal cells divided once or twice and then accumulated in G1. These results are best explained by a two-stage model for cellular senescence. Mortality stage 1 (M1) causes a loss of mitogen responsiveness and arrest near the G1/S interface and can be bypassed or overcome by the cellular DNA synthesis-stimulating activity of T antigen. Mortality stage 2 (M2) is an independent mechanism that is responsible for the failure of cell division during crisis. The inactivation of M2 is a rare event, probably of mutational origin in human cells, independent of or only indirectly related to the expression of T antigen. Under this hypothesis, T-antigen-immortalized cells contain an active but bypassed M1 mechanism and an inactivated M2 mechanism. These cells are dependent on the continued expression of T antigen for the maintenance of immortality for the same reason that precrisis cells are dependent on T antigen for growth: both contain an active M1 mechanism.},
author = {Wright, W E and Pereira-Smith, O M and Shay, J W},
doi = {10.1128/MCB.9.7.3088},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Wright, Pereira-Smith, Shay - 1989 - Reversible cellular senescence implications for immortalization of normal human diploid fibroblasts.pdf:pdf},
isbn = {0270-7306 (Print)$\backslash$r0270-7306 (Linking)},
issn = {0270-7306},
journal = {Mol. Cell. Biol.},
keywords = {Antigens,Biological,Cell Division,Cell Division: drug effects,Cell Line,Cell Survival,Cell Transformation,Dexamethasone,Dexamethasone: pharmacology,Diploidy,Fibroblasts,Fibroblasts: cytology,Fibroblasts: drug effects,Fibroblasts: physiology,Fibroblasts: ultrastructure,Humans,Interphase,Models,Plasmids,Polyomavirus Transforming,Polyomavirus Transforming: genetics,Polyomavirus Transforming: physiology,Transfection,Viral,cancer,immortalization},
mendeley-tags = {cancer,immortalization},
number = {7},
pages = {3088--3092},
pmid = {2779554},
title = {{Reversible cellular senescence: implications for immortalization of normal human diploid fibroblasts.}},
volume = {9},
year = {1989}
}
@article{Langfelder2008,
author = {Langfelder, Peter and Horvath, Steve},
doi = {10.1186/1471-2105-9-559},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Langfelder, Horvath - 2008 - WGCNA an R package for weighted correlation network analysis.pdf:pdf},
journal = {BMC Bioinformatics},
pages = {559},
title = {{WGCNA : an R package for weighted correlation network analysis}},
volume = {9},
year = {2008}
}
@article{Renehan2006,
abstract = {Accumulating epidemiological evidence shows that being either overweight or obese, in other words having excess body weight (EBW), is associated with an increased risk of several, common, adult cancers. The molecular mechanisms that underlie these associations are not understood fully, but insulin resistance is likely to be important. The insulin-cancer hypothesis postulates that chronic hyperinsulinemia is associated with decreased concentrations of insulin-like growth factor binding protein1 (IGFBP-1) and IGFBP-2, leading to increased availability of IGF-I and concomitant changes in the cellular environment that favor tumor formation. However, the situation is likely to be more complex because hyperinsulinemia is also associated with alterations in related molecular systems (e.g. sex steroids and adipocytokines). As the prevalence of EBW increases to epidemic proportions, untangling the links between EBW and the insulin-IGF axis and its wider molecular interactions will become increasingly important in the development of preventive strategies. ?? 2006 Elsevier Ltd. All rights reserved.},
author = {Renehan, Andrew G. and Frystyk, Jan and Flyvbjerg, Allan},
doi = {10.1016/j.tem.2006.08.006},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Renehan, Frystyk, Flyvbjerg - 2006 - Obesity and cancer risk the role of the insulin-IGF axis.pdf:pdf},
isbn = {1043-2760 (Print)},
issn = {10432760},
journal = {Trends Endocrinol. Metab.},
keywords = {obesity and cancer},
mendeley-tags = {obesity and cancer},
number = {8},
pages = {328--336},
pmid = {16956771},
title = {{Obesity and cancer risk: the role of the insulin-IGF axis}},
volume = {17},
year = {2006}
}
@article{Lumeng2011,
abstract = {The obesity epidemic has forced us to evaluate the role of inflammation in the health complications of obesity. This has led to a convergence of the fields of immunology and nutrient physiology and the understanding that they are inextricably linked. The reframing of obesity as an inflammatory condition has had a wide impact on our concep- tualization of obesity-associated diseases. In this Review, we highlight the cellular and molecular mechanisms at play in the generation of obesity-induced inflammation. We also emphasize how defining the immune regulation in metabolic tissues has broadened the understanding of the diversity of inflammatory responses.},
author = {Lumeng, Carey N and Saltiel, Alan R},
doi = {10.1172/JCI57132.In},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Lumeng, Saltiel - 2011 - Inflammatory links between obesity and metabolic disease.pdf:pdf},
isbn = {0021-9738},
issn = {00219738},
journal = {J. Clin. Invest.},
keywords = {inflammation,obesity},
mendeley-tags = {inflammation,obesity},
number = {6},
pages = {2111--2117},
pmid = {21633179},
title = {{Inflammatory links between obesity and metabolic disease}},
volume = {121},
year = {2011}
}
@article{Khatri2012,
abstract = {Pathway analysis has become the first choice for gaining insight into the underlying biology of differentially expressed genes and proteins, as it reduces complexity and has increased explanatory power. We discuss the evolution of knowledge base-driven pathway analysis over its first decade, distinctly divided into three generations. We also discuss the limitations that are specific to each generation, and how they are addressed by successive generations of methods. We identify a number of annotation challenges that must be addressed to enable development of the next generation of pathway analysis methods. Furthermore, we identify a number of methodological challenges that the next generation of methods must tackle to take advantage of the technological advances in genomics and proteomics in order to improve specificity, sensitivity, and relevance of pathway analysis.},
author = {Khatri, Purvesh and Sirota, Marina and Butte, Atul J.},
doi = {10.1371/journal.pcbi.1002375},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Khatri, Sirota, Butte - 2012 - Ten years of pathway analysis Current approaches and outstanding challenges.pdf:pdf},
isbn = {1553-7358 (Electronic)$\backslash$r1553-734X (Linking)},
issn = {1553734X},
journal = {PLoS Comput. Biol.},
number = {2},
pmid = {22383865},
title = {{Ten years of pathway analysis: Current approaches and outstanding challenges}},
volume = {8},
year = {2012}
}
@article{Lawrence2013,
abstract = {Major international projects are underway that are aimed at creating a comprehensive catalogue of all the genes responsible for the initiation and progression of cancer. These studies involve the sequencing of matched tumour-normal samples followed by mathematical analysis to identify those genes in which mutations occur more frequently than expected by random chance. Here we describe a fundamental problem with cancer genome studies: as the sample size increases, the list of putatively significant genes produced by current analytical methods burgeons into the hundreds. The list includes many implausible genes (such as those encoding olfactory receptors and the muscle protein titin), suggesting extensive false-positive findings that overshadow true driver events. We show that this problem stems largely from mutational heterogeneity and provide a novel analytical methodology, MutSigCV, for resolving the problem. We apply MutSigCV to exome sequences from 3,083 tumour-normal pairs and discover extraordinary variation in mutation frequency and spectrum within cancer types, which sheds light on mutational processes and disease aetiology, and in mutation frequency across the genome, which is strongly correlated with DNA replication timing and also with transcriptional activity. By incorporating mutational heterogeneity into the analyses, MutSigCV is able to eliminate most of the apparent artefactual findings and enable the identification of genes truly associated with cancer.},
author = {Lawrence, Michael S and Stojanov, Petar and Polak, Paz and Kryukov, Gregory V and Cibulskis, Kristian and Sivachenko, Andrey and Carter, Scott L and Stewart, Chip and Mermel, Craig H and Roberts, Steven A and Kiezun, Adam and Hammerman, Peter S and McKenna, Aaron and Drier, Yotam and Zou, Lihua and Ramos, Alex H and Pugh, Trevor J and Stransky, Nicolas and Helman, Elena and Kim, Jaegil and Sougnez, Carrie and Ambrogio, Lauren and Nickerson, Elizabeth and Shefler, Erica and Cort{\'{e}}s, Maria L and Auclair, Daniel and Saksena, Gordon and Voet, Douglas and Noble, Michael and DiCara, Daniel and Lin, Pei and Lichtenstein, Lee and Heiman, David I and Fennell, Timothy and Imielinski, Marcin and Hernandez, Bryan and Hodis, Eran and Baca, Sylvan and Dulak, Austin M and Lohr, Jens and Landau, Dan-Avi and Wu, Catherine J and Melendez-Zajgla, Jorge and Hidalgo-Miranda, Alfredo and Koren, Amnon and McCarroll, Steven A and Mora, Jaume and Lee, Ryan S and Crompton, Brian and Onofrio, Robert and Parkin, Melissa and Winckler, Wendy and Ardlie, Kristin and Gabriel, Stacey B and Roberts, Charles W M and Biegel, Jaclyn A and Stegmaier, Kimberly and Bass, Adam J and Garraway, Levi A and Meyerson, Matthew and Golub, Todd R and Gordenin, Dmitry A and Sunyaev, Shamil and Lander, Eric S and Getz, Gad},
doi = {10.1038/nature12213},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Lawrence et al.{\_}2013{\_}Mutational heterogeneity in cancer and the search for new cancer-associated genes.pdf:pdf},
isbn = {1476-4687 (Electronic)$\backslash$r0028-0836 (Linking)},
issn = {1476-4687},
journal = {Nature},
keywords = {Artifacts,DNA Replication Timing,Exome,Exome: genetics,False Positive Reactions,Gene Expression,Genetic Heterogeneity,Genome,Human,Human: genetics,Humans,Lung Neoplasms,Lung Neoplasms: genetics,Mutation,Mutation Rate,Mutation: genetics,Neoplasms,Neoplasms: classification,Neoplasms: genetics,Neoplasms: pathology,Oncogenes,Oncogenes: genetics,Reproducibility of Results,Sample Size,Squamous Cell,Squamous Cell: genetics},
number = {7457},
pages = {214--218},
pmid = {23770567},
title = {{Mutational heterogeneity in cancer and the search for new cancer-associated genes.}},
volume = {499},
year = {2013}
}
@article{Frayling2007,
abstract = {Obesity is a serious international health problem that increases the risk of several common diseases. The genetic factors predisposing to obesity are poorly understood. A genome-wide search for type 2 diabetes–susceptibility genes identified a common variant in the FTO (fat mass and obesity associated) gene that predisposes to diabetes through an effect on body mass index (BMI). An additive association of the variant with BMI was replicated in 13 cohorts with 38,759 participants. The 16{\%} of adults who are homozygous for the risk allele weighed about 3 kilograms more and had 1.67-fold increased odds of obesity when compared with those not inheriting a risk allele. This association was observed from age 7 years upward and reflects a specific increase in fat mass.},
author = {Frayling, Timothy M. and Timpson, Nicholas J and Weedon, Michael N and Freathy, Rachel M and Lindgren, Cecilia M and Perry, John R B and Katherine, S and Lango, Hana and Rayner, Nigel W and Shields, Beverley and Harries, Lorna W and Barrett, C and Ellard, Sian and Groves, Christopher J and Knight, Bridget and Patch, Ann-marie and Ness, Andrew R and Ebrahim, Shah and Lawlor, Debbie a and Ring, Susan M and Ben-shlomo, Yoav and Jarvelin, Marjo-riitta and Sovio, Ulla and Bennett, Amanda J and Melzer, David and Loos, Ruth J F and Barroso, In{\^{e}}s and Wareham, Nicholas J and Karpe, Fredrik and Owen, Katharine R and Cardon, Lon R and Walker, Mark and Hitman, Graham a and Colin, N a and Doney, Alex S F and Morris, Andrew D and Smith, George Davey and Wellcome, The and Case, Trust and Consortium, Control and Hattersley, Andrew T and Mccarthy, Mark I},
doi = {10.1126/science.1141634},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Frayling et al. - 2007 - A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obes.pdf:pdf},
isbn = {1095-9203 (Electronic)},
issn = {0036-8075},
journal = {Science (80-. ).},
keywords = {FTO,GWAS,obesity},
mendeley-tags = {FTO,GWAS,obesity},
pages = {889--894},
pmid = {17434869},
title = {{A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity}},
volume = {316},
year = {2007}
}
@article{Batterham2002,
abstract = {Food intake is regulated by the hypothalamus, including the melanocortin and neuropeptide Y (NPY) systems in the arcuate nucleus. The NPY Y2 receptor (Y2R), a putative inhibitory presynaptic receptor, is highly expressed on NPY neurons in the arcuate nucleus, which is accessible to peripheral hormones. Peptide YY(3-36) (PYY(3-36)), a Y2R agonist, is released from the gastrointestinal tract postprandially in proportion to the calorie content of a meal. Here we show that peripheral injection of PYY(3-36) in rats inhibits food intake and reduces weight gain. PYY(3-36) also inhibits food intake in mice but not in Y2r-null mice, which suggests that the anorectic effect requires the Y2R. Peripheral administration of PYY(3-36) increases c-Fos immunoreactivity in the arcuate nucleus and decreases hypothalamic Npy messenger RNA. Intra-arcuate injection of PYY(3-36) inhibits food intake. PYY(3-36) also inhibits electrical activity of NPY nerve terminals, thus activating adjacent pro-opiomelanocortin (POMC) neurons. In humans, infusion of normal postprandial concentrations of PYY(3-36) significantly decreases appetite and reduces food intake by 33{\%} over 24 h. Thus, postprandial elevation of PYY(3-36) may act through the arcuate nucleus Y2R to inhibit feeding in a gut-hypothalamic pathway.},
author = {Batterham, Rachel L and Cowley, Michael a and Small, Caroline J and Herzog, Herbert and Cohen, Mark a and Dakin, Catherine L and Wren, Alison M and Brynes, Audrey E and Low, Malcolm J and Ghatei, Mohammad a and Cone, Roger D and Bloom, Stephen R},
doi = {10.1038/nature00887},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Batterham et al. - 2002 - Gut hormone PYY(3-36) physiologically inhibits food intake.pdf:pdf},
isbn = {0028-0836 (Print)$\backslash$r0028-0836 (Linking)},
issn = {0028-0836},
journal = {Nature},
keywords = {obesity},
mendeley-tags = {obesity},
number = {6898},
pages = {650--654},
pmid = {12167864},
title = {{Gut hormone PYY(3-36) physiologically inhibits food intake.}},
volume = {418},
year = {2002}
}
@article{Boffetta2003,
abstract = {Environmental carcinogens, in a strict sense, include outdoor and indoor air pollutants, as well as soil and drinking water contaminants. An increased risk of mesothelioma has consistently been detected among individuals experiencing residential exposure to asbestos, whereas results for lung cancer are less consistent. At least 14 good-quality studies have investigated lung cancer risk from outdoor air pollution based on measurement of specific agents. Their results tend to show an increased risk in the categories at highest exposure, with relative risks in the range 1.5-2.0, which is not attributable to confounders. Results for other cancers are sparse. A causal association has been established between exposure to environmental tobacco smoke and lung cancer, with a relative risk in the order of 1.2. Radon is another carcinogen present in indoor air which may be responsible for 1{\%} of all lung cancers. In several Asian populations, an increased risk of lung cancer is present in women from indoor pollution from cooking and heating. There is strong evidence of an increased risk of bladder, skin and lung cancers following consumption of water with high arsenic contamination; results for other drinking water contaminants, including chlorination by-products, are inconclusive. A precise quantification of the burden of human cancer attributable to environmental exposure is problematic. However, despite the relatively small relative risks of cancer following exposure to environmental carcinogens, the number of cases that might be caused, assuming a causal relationship, is relatively large, as a result of the high prevalence of exposure.},
author = {Boffetta, P and Nyberg, F},
doi = {10.1093/bmb/ldg023},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Boffetta, Nyberg - 2003 - Contribution of environmental factors to cancer risk.pdf:pdf},
isbn = {0007-1420 (Print)$\backslash$r0007-1420 (Linking)},
journal = {Br Med Bull},
keywords = {Air Pollution/adverse effects,Arsenic/toxicity,Asbestos/toxicity,Environmental Exposure/adverse effects,Environmental Pollutants/ toxicity,Humans,Neoplasms/ chemically induced,Radon/toxicity,Risk Factors,Tobacco Smoke Pollution/adverse effects,Water Purification,Water Supply,cancer,environmental factors},
mendeley-tags = {cancer,environmental factors},
pages = {71--94},
pmid = {14757710},
title = {{Contribution of environmental factors to cancer risk}},
volume = {68},
year = {2003}
}
@article{Pate1995,
author = {Pate, Russell R and Pratt, Michael and Blair, Steven N and Haskell, William L and Macera, Caroline A and Bouchard, Claude and Buchner, David and Ettinger, Walter and Heath, Gregory W and King, Abby C and Kriska, Andrea and Leon, Arthur S and Marcus, Bess H and Morris, Jeremy and Paffenbarger, Ralph S and Patrick, Kevin and Pollock, Michael L and Rippe, James M and Sallis, James and Wilmore, Jack H},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Pate et al. - 1995 - Physical activity and public health A recommendation from the Centers for Disease Control and prevention and the Am.pdf:pdf},
journal = {J. Am. Med. Assoc.},
keywords = {obesity},
mendeley-tags = {obesity},
number = {5},
pages = {402--407},
title = {{Physical activity and public health: A recommendation from the Centers for Disease Control and prevention and the American College of Sports Medicine}},
volume = {273},
year = {1995}
}
@article{Calle2004,
abstract = {The prevalence of obesity is rapidly increasing globally. Epidemiological studies have associated obesity with a range of cancer types, although the mechanisms by which obesity induces or promotes tumorigenesis vary by cancer site. These include insulin resistance and resultant chronic hyperinsulinaemia, increased bioavailability of steroid hormones and localized inflammation. Gaining a better understanding of the relationship between obesity and cancer can provide new insight into mechanisms of cancer pathogenesis.},
author = {Calle, Eugenia E and Kaaks, Rudolf},
doi = {10.1038/nrc1408},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Calle, Kaaks - 2004 - Overweight, obesity and cancer epidemiological evidence and proposed mechanisms.pdf:pdf},
isbn = {1474-175X (Print)$\backslash$r1474-175X (Linking)},
issn = {1474-175X},
journal = {Nat. Rev. Cancer},
keywords = {cancer,environmental factors},
mendeley-tags = {cancer,environmental factors},
number = {8},
pages = {579--591},
pmid = {15286738},
title = {{Overweight, obesity and cancer: epidemiological evidence and proposed mechanisms.}},
volume = {4},
year = {2004}
}
@article{Moelling2002,
abstract = {We have recently shown that the Ras-Raf-MEK-ERK and phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathways can cross-talk in the human breast cancer cell line MCF-7. High Raf activity induces growth arrest and differentiation in these cells, whereas high PI3K/Akt activity correlates with cell survival and proliferation. Here we show that the Raf-Akt cross-talk is regulated in a concentration- and ligand-dependent manner. High doses of insulin-like growth factor I (IGF-I) activate Akt quickly and strongly enough to suppress Raf kinase activity via phosphorylation of Ser-259, whereas low doses of IGF-I do not trigger this cross-talk but are still mitogenic. Phorbol 12-myristate 13-acetate, a differentiation-inducing stimulus, potently activates the Ras-Raf-MEK-ERK pathway but only weakly activates PI3K/Akt and does not trigger the cross-talk. Thus, the herein analyzed parameters such as ligand type, concentration, and time course may contribute to the cellular response of either proliferation or differentiation. This is highly relevant to understanding cellular transformation and may be of use in areas like tissue engineering.},
author = {Moelling, Karin and Schad, Karen and Bosse, Magnus and Zimmermann, Sven and Schweneker, Marc},
doi = {10.1074/jbc.M111974200},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Moelling et al. - 2002 - Regulation of Raf-Akt cross-talk.pdf:pdf},
isbn = {0021-9258 (Print)},
issn = {00219258},
journal = {J. Biol. Chem.},
keywords = {Raf/Akt crosstalk,cancer},
mendeley-tags = {Raf/Akt crosstalk,cancer},
number = {34},
pages = {31099--31106},
pmid = {12048182},
title = {{Regulation of Raf-Akt cross-talk}},
volume = {277},
year = {2002}
}
@article{Damrauer2014,
abstract = {We sought to define whether there are intrinsic molecular subtypes of high-grade bladder cancer. Consensus clustering performed on gene expression data from a meta-dataset of high-grade, muscle-invasive bladder tumors identified two intrinsic, molecular subsets of high-grade bladder cancer, termed "luminal" and "basal-like," which have characteristics of different stages of urothelial differentiation, reflect the luminal and basal-like molecular subtypes of breast cancer, and have clinically meaningful differences in outcome. A gene set predictor, bladder cancer analysis of subtypes by gene expression (BASE47) was defined by prediction analysis of microarrays (PAM) and accurately classifies the subtypes. Our data demonstrate that there are at least two molecularly and clinically distinct subtypes of high-grade bladder cancer and validate the BASE47 as a subtype predictor. Future studies exploring the predictive value of the BASE47 subtypes for standard of care bladder cancer therapies, as well as novel subtype-specific therapies, will be of interest.},
author = {Damrauer, J S and Hoadley, K A and Chism, D D and Fan, C and Tiganelli, C J and Wobker, S E and Yeh, J J and Milowsky, M I and Iyer, G and Parker, J S and Kim, W Y},
doi = {10.1073/pnas.1318376111},
file = {:Users/rikutakei/Downloads/PNAS-2014-Damrauer-3110-5.pdf:pdf},
isbn = {1091-6490 (Electronic)$\backslash$r0027-8424 (Linking)},
issn = {1091-6490},
journal = {Proc. Natl. Acad. Sci. U. S. A.},
keywords = {*Models,Biological,Breast Neoplasms/classification,Cluster Analysis,Gene Expression Profiling/methods,Gene Expression Regulation,Humans,Microarray Analysis,Neoplastic/*genetics,Predictive Value of Tests,Urinary Bladder Neoplasms/*classification/*genetic},
number = {8},
pages = {3110--3115},
pmid = {24520177},
title = {{Intrinsic subtypes of high-grade bladder cancer reflect the hallmarks of breast cancer biology}},
volume = {111},
year = {2014}
}
@article{Kopelman2007,
abstract = {The article presents that overweight and obesity can cause health problems and they are significant contributors of ill health. The role of cytokines, insulin resistance and pro-inflammatory markers in the development of health risks is mentioned. Health risks associated with obesity include congestive cardiac failure, sleep breathing abnormalities and alterations in cardiac function.},
author = {Kopelman, P},
doi = {10.1111/j.1467-789X.2007.00311.x},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Kopelman - 2007 - Health risks associated with overweight and obesity.pdf:pdf},
isbn = {1467-789X},
issn = {1467-7881},
journal = {Obes. Rev.},
keywords = {obesity,obesity risk},
mendeley-tags = {obesity risk},
pages = {13--17},
pmid = {17316295},
title = {{Health risks associated with overweight and obesity.}},
volume = {8},
year = {2007}
}
@article{Zhang1994,
author = {Zhang, Yiying and Proenca, Ricardo and Maffei, Margherita and Barone, Marisa and Leopold, Lori and Friedman, Jeffrey M},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Zhang et al. - 1994 - Positional cloning of the mouse obese gene and its human homologue.pdf:pdf},
journal = {Nature},
keywords = {obesity},
mendeley-tags = {obesity},
pages = {425--432},
title = {{Positional cloning of the mouse obese gene and its human homologue}},
volume = {372},
year = {1994}
}
@article{Farooqi2003,
author = {Farooqi, I. Sadaf and Keogh, Julia M. and Yeo, Giles S. H. and Lank, Emma J. and Cheetham, Tim and O'Rahilly, Stephen},
doi = {10.1056/NEJMoa0810625)},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Farooqi et al. - 2003 - Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene.pdf:pdf},
journal = {N. Engl. J. Med.},
keywords = {obesity},
mendeley-tags = {obesity},
number = {12},
pages = {1085--1095},
title = {{Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene}},
volume = {348},
year = {2003}
}
@misc{Neuwirth2014,
author = {Neuwirth, E},
title = {{RColorBrewer: ColorBrewer Palettes}},
year = {2014}
}
@article{Hanahan2011,
abstract = {The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list - reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. ?? 2011 Elsevier Inc.},
author = {Hanahan, Douglas and Weinberg, Robert A.},
doi = {10.1016/j.cell.2011.02.013},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Hanahan, Weinberg{\_}2011{\_}Hallmarks of cancer The next generation.pdf:pdf},
isbn = {0026201009680},
issn = {00928674},
journal = {Cell},
keywords = {Key Paper},
mendeley-tags = {Key Paper},
number = {5},
pages = {646--674},
pmid = {21376230},
publisher = {Elsevier Inc.},
title = {{Hallmarks of cancer: The next generation}},
volume = {144},
year = {2011}
}
@misc{R2016,
author = {{R Development Core Team}},
title = {{R: A language and environment for statictical computing}},
url = {https://www.r-project.org/},
urldate = {2016-01-09},
year = {2016}
}
@article{Smemo2014a,
abstract = {Genome-wide association studies (GWAS) have reproducibly associated variants within introns of FTO with increased risk for obesity and type 2 diabetes (T2D). Although the molecular mechanisms linking these noncoding variants with obesity are not immediately obvious, subsequent studies in mice demonstrated that FTO expression levels influence body mass and composition phenotypes. However, no direct connection between the obesity-associated variants and FTO expression or function has been made. Here we show that the obesity-associated noncoding sequences within FTO are functionally connected, at megabase distances, with the homeobox gene IRX3. The obesity-associated FTO region directly interacts with the promoters of IRX3 as well as FTO in the human, mouse and zebrafish genomes. Furthermore, long-range enhancers within this region recapitulate aspects of IRX3 expression, suggesting that the obesity-associated interval belongs to the regulatory landscape of IRX3. Consistent with this, obesity-associated single nucleotide polymorphisms are associated with expression of IRX3, but not FTO, in human brains. A direct link between IRX3 expression and regulation of body mass and composition is demonstrated by a reduction in body weight of 25 to 30{\%} in Irx3-deficient mice, primarily through the loss of fat mass and increase in basal metabolic rate with browning of white adipose tissue. Finally, hypothalamic expression of a dominant-negative form of Irx3 reproduces the metabolic phenotypes of Irx3-deficient mice. Our data suggest that IRX3 is a functional long-range target of obesity-associated variants within FTO and represents a novel determinant of body mass and composition.},
archivePrefix = {arXiv},
arxivId = {NIHMS150003},
author = {Smemo, Scott and Tena, Juan J and Kim, Kyoung-Han and Gamazon, Eric R and Sakabe, Noboru J and G{\'{o}}mez-Mar{\'{i}}n, Carlos and Aneas, Ivy and Credidio, Flavia L and Sobreira, D{\'{e}}bora R and Wasserman, Nora F and Lee, Ju Hee and Puviindran, Vijitha and Tam, Davis and Shen, Michael and Son, Joe Eun and Vakili, Niki Alizadeh and Sung, Hoon-Ki and Naranjo, Silvia and Acemel, Rafael D and Manzanares, Miguel and Nagy, Andras and Cox, Nancy J and Hui, Chi-Chung and Gomez-Skarmeta, Jose Luis and N{\'{o}}brega, Marcelo a},
doi = {10.1038/nature13138},
eprint = {NIHMS150003},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Smemo et al. - 2014 - Obesity-associated variants within FTO form long-range functional connections with IRX3.pdf:pdf},
isbn = {1476-4687 (Electronic)$\backslash$r0028-0836 (Linking)},
issn = {1476-4687},
journal = {Nature},
keywords = {Adipose Tissue,Adipose Tissue: metabolism,Animals,Basal Metabolism,Basal Metabolism: genetics,Body Mass Index,Body Weight,Body Weight: genetics,Brain,Brain: metabolism,Diabetes Mellitus,Diet,Dominant,Dominant: genetics,FTO,Genes,Genetic,Genetic: genetics,Homeodomain Proteins,Homeodomain Proteins: genetics,Homeodomain Proteins: metabolism,Humans,Hypothalamus,Hypothalamus: metabolism,Introns,Introns: genetics,Male,Mice,Mixed Function Oxygenases,Mixed Function Oxygenases: genetics,Obesity,Obesity: genetics,Oxo-Acid-Lyases,Oxo-Acid-Lyases: genetics,Phenotype,Polymorphism,Promoter Regions,Proteins,Proteins: genetics,Single Nucleotide,Single Nucleotide: genetics,Thinness,Thinness: genetics,Transcription Factors,Transcription Factors: deficiency,Transcription Factors: genetics,Transcription Factors: metabolism,Type 2,Type 2: genetics,Zebrafish,Zebrafish: embryology,Zebrafish: genetics},
mendeley-tags = {FTO},
number = {7492},
pages = {371--375},
pmid = {24646999},
title = {{Obesity-associated variants within FTO form long-range functional connections with IRX3.}},
volume = {507},
year = {2014}
}
@article{Lawrence2014,
abstract = {Although a few cancer genes are mutated in a high proportion of tumours of a given type ({\textgreater}20{\%}), most are mutated at intermediate frequencies (2-20{\%}). To explore the feasibility of creating a comprehensive catalogue of cancer genes, we analysed somatic point mutations in exome sequences from 4,742 human cancers and their matched normal-tissue samples across 21 cancer types. We found that large-scale genomic analysis can identify nearly all known cancer genes in these tumour types. Our analysis also identified 33 genes that were not previously known to be significantly mutated in cancer, including genes related to proliferation, apoptosis, genome stability, chromatin regulation, immune evasion, RNA processing and protein homeostasis. Down-sampling analysis indicates that larger sample sizes will reveal many more genes mutated at clinically important frequencies. We estimate that near-saturation may be achieved with 600-5,000 samples per tumour type, depending on background mutation frequency. The results may help to guide the next stage of cancer genomics.},
author = {Lawrence, Michael S and Stojanov, Petar and Mermel, Craig H and Robinson, James T and Garraway, Levi A and Golub, Todd R and Meyerson, Matthew and Gabriel, Stacey B and Lander, Eric S and Getz, Gad},
doi = {10.1038/nature12912},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Lawrence et al.{\_}2014{\_}Discovery and saturation analysis of cancer genes across 21 tumour types.pdf:pdf},
isbn = {1476-4687 (Electronic)$\backslash$r0028-0836 (Linking)},
issn = {1476-4687},
journal = {Nature},
keywords = {Apoptosis,Apoptosis: genetics,Case-Control Studies,Cell Proliferation,Chromatin,Chromatin: genetics,DNA Mutational Analysis,Exome,Exome: genetics,Genes,Genome,Genomic Instability,Genomic Instability: genetics,Genomics,Human,Human: genetics,Humans,Immune Evasion,Immune Evasion: genetics,Mutation Rate,Neoplasm,Neoplasm: genetics,Neoplasms,Neoplasms: classification,Neoplasms: genetics,Neoplasms: pathology,Point Mutation,Point Mutation: genetics,Post-Transcriptional,Post-Transcriptional: genetics,RNA Processing,Sample Size},
number = {7484},
pages = {495--501},
pmid = {24390350},
publisher = {Nature Publishing Group},
title = {{Discovery and saturation analysis of cancer genes across 21 tumour types.}},
volume = {505},
year = {2014}
}
@article{GO2004,
abstract = {The Gene Ontology (GO) project (http://www. geneontology.org/) provides structured, controlled vocabularies and classifications that cover several domains of molecular and cellular biology and are freely available for community use in the annotation of genes, gene products and sequences. Many model organism databases and genome annotation groups use the GO and contribute their annotation sets to the GO resource. The GO database integrates the vocabularies and contributed annotations and provides full access to this information in several formats. Members of the GO Consortium continually work collectively, involving outside experts as needed, to expand and update the GO vocabularies. The GO Web resource also provides access to extensive documentation about the GO project and links to applications that use GO data for functional analyses.},
author = {{Gene Ontology Consortium}},
doi = {10.1093/nar/gkh036},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Gene Ontology Consortium - 2004 - The Gene Ontology (GO) database and informatics resource.pdf:pdf},
isbn = {1362-4962 (Electronic)},
issn = {1362-4962},
journal = {Nucleic Acids Res.},
number = {Database issue},
pages = {258D--261},
pmid = {14681407},
title = {{The Gene Ontology (GO) database and informatics resource.}},
volume = {32},
year = {2004}
}
@misc{ICGC,
author = {{International Cancer Genome Consortium}},
title = {{International Cancer Genome Consortium}},
url = {http://icgc.org/},
urldate = {7/9/2015},
year = {2016}
}
@misc{WHO2016,
author = {{World Health Organisation}},
title = {{Cancer factsheet}},
url = {http://www.who.int/mediacentre/factsheets/fs297/en/},
urldate = {2016-11-16},
year = {2016}
}
@article{Kojima1999,
abstract = {Small synthetic molecules called growth-hormone secretagogues (GHSs) stimulate the release of growth hormone (GH) from the pituitary. They act through GHS-R, a G-protein-coupled receptor for which the ligand is unknown. Recent cloning of GHS-R strongly suggests that an endogenous ligand for the receptor does exist and that there is a mechanism for regulating GH release that is distinct from its regulation by hypothalamic growth-hormone-releasing hormone (GHRH). We now report the purification and identification in rat stomach of an endogenous ligand specific for GHS-R. The purified ligand is a peptide of 28 amino acids, in which the serine 3 residue is n-octanoylated. The acylated peptide specifically releases GH both in vivo and in vitro, and O-n-octanoylation at serine 3 is essential for the activity. We designate the GH-releasing peptide 'ghrelin' (ghre is the Proto-Indo-European root of the word 'grow'). Human ghrelin is homologous to rat ghrelin apart from two amino acids. The occurrence of ghrelin in both rat and human indicates that GH release from the pituitary may be regulated not only by hypothalamic GHRH, but also by ghrelin.},
author = {Kojima, M and Hosoda, H and Date, Y and Nakazato, M and Matsuo, H and Kangawa, K},
doi = {10.1038/45230},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Kojima et al. - 1999 - Ghrelin is a growth-hormone-releasing acylated peptide from stomach.pdf:pdf},
isbn = {0028-0836},
issn = {0028-0836},
journal = {Nature},
number = {6762},
pages = {656--660},
pmid = {10604470},
title = {{Ghrelin is a growth-hormone-releasing acylated peptide from stomach}},
volume = {402},
year = {1999}
}
@article{Schulze2001,
abstract = {Parallel quantification of large numbers of messenger RNA transcripts using microarray technology promises to provide detailed insight into cellular processes involved in the regulation of gene expression. This should allow new understanding of signalling networks that operate in the cell and of the molecular basis and classification of disease. But can the technology deliver such far-reaching promises?},
author = {Schulze, Almut and Downward, Julian},
doi = {10.1038/35087138},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Schulze, Downward - 2001 - Navigating gene expression using microarrays--a technology review.pdf:pdf},
isbn = {1465-7392},
issn = {1465-7392},
journal = {Nat. Cell Biol.},
number = {8},
pages = {E190--E195},
pmid = {11483980},
title = {{Navigating gene expression using microarrays--a technology review.}},
volume = {3},
year = {2001}
}
@article{Scuteri2007,
abstract = {The obesity epidemic is responsible for a substantial economic burden in developed countries and is a major risk factor for type 2 diabetes and cardiovascular disease. The disease is the result not only of several environmental risk factors, but also of genetic predisposition. To take advantage of recent advances in gene-mapping technology, we executed a genome-wide association scan to identify genetic variants associated with obesity-related quantitative traits in the genetically isolated population of Sardinia. Initial analysis suggested that several SNPs in the FTO and PFKP genes were associated with increased BMI, hip circumference, and weight. Within the FTO gene, rs9930506 showed the strongest association with BMI (p = 8.6 x10(-7)), hip circumference (p = 3.4 x 10(-8)), and weight (p = 9.1 x 10(-7)). In Sardinia, homozygotes for the rare "G" allele of this SNP (minor allele frequency = 0.46) were 1.3 BMI units heavier than homozygotes for the common "A" allele. Within the PFKP gene, rs6602024 showed very strong association with BMI (p = 4.9 x 10(-6)). Homozygotes for the rare "A" allele of this SNP (minor allele frequency = 0.12) were 1.8 BMI units heavier than homozygotes for the common "G" allele. To replicate our findings, we genotyped these two SNPs in the GenNet study. In European Americans (N = 1,496) and in Hispanic Americans (N = 839), we replicated significant association between rs9930506 in the FTO gene and BMI (p-value for meta-analysis of European American and Hispanic American follow-up samples, p = 0.001), weight (p = 0.001), and hip circumference (p = 0.0005). We did not replicate association between rs6602024 and obesity-related traits in the GenNet sample, although we found that in European Americans, Hispanic Americans, and African Americans, homozygotes for the rare "A" allele were, on average, 1.0-3.0 BMI units heavier than homozygotes for the more common "G" allele. In summary, we have completed a whole genome-association scan for three obesity-related quantitative traits and report that common genetic variants in the FTO gene are associated with substantial changes in BMI, hip circumference, and body weight. These changes could have a significant impact on the risk of obesity-related morbidity in the general population.},
author = {Scuteri, Angelo and Sanna, Serena and Chen, Wei Min and Uda, Manuela and Albai, Giuseppe and Strait, James and Najjar, Samer and Nagaraja, Ramaiah and Orr??, Marco and Usala, Gianluca and Dei, Mariano and Lai, Sandra and Maschio, Andrea and Busonero, Fabio and Mulas, Antonella and Ehret, Georg B. and Fink, Ashley A. and Weder, Alan B. and Cooper, Richard S. and Galan, Pilar and Chakravarti, Aravinda and Schlessinger, David and Cao, Antonio and Lakatta, Edward and Abecasis, Gon??alo R.},
doi = {10.1371/journal.pgen.0030115},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Scuteri et al. - 2007 - Genome-wide association scan shows genetic variants in the FTO gene are associated with obesity-related traits.pdf:pdf},
isbn = {1553-7404},
issn = {15537390},
journal = {PLoS Genet.},
keywords = {FTO,GWAS,obesity},
mendeley-tags = {FTO,GWAS,obesity},
number = {7},
pages = {1200--1210},
pmid = {17658951},
title = {{Genome-wide association scan shows genetic variants in the FTO gene are associated with obesity-related traits}},
volume = {3},
year = {2007}
}
@article{Arem2013,
abstract = {Background Higher body mass index (BMI) and inactivity have been associated with a higher risk of developing endometrial cancer, but the impact on endometrial cancer survival is unclear. Methods Among incident endometrial cancer case subjects in the National Institutes of Health-AARP Diet and Health Study, we examined associations of prediagnosis BMI (n = 1400) and physical activity (n = 875) with overall and disease-specific 5- and 10-year mortality. Using Cox proportional hazards regression, we estimated hazard ratios (HRs) and 95{\%} confidence intervals (CIs), adjusting for tumor characteristics, treatment, and other risk factors. All statistical tests were two-sided. Results Compared with women with a BMI in the range of 18.5 to less than 25kg/m(2), the hazard ratios for 5-year all-cause mortality were 1.74 (95{\%} CI = 1.13 to 2.66) for BMI in the range of 25 to less than 30kg/m(2), 1.84 (95{\%} CI = 1.17 to 2.88) for BMI in the range of 30 to less than 35kg/m(2), and 2.35 (95{\%} CI = 1.48 to 3.73) for BMI greater than or equal to 35kg/m(2) (P trend {\textless} .001). Higher BMI was also statistically significantly associated with poorer endometrial cancer-specific but not cardiovascular disease 5-year mortality. Hazard ratio estimates for 10-year all-cause and endometrial cancer-specific mortality as related to BMI were similar to 5-year hazard ratio estimates, whereas 10-year cardiovascular disease mortality became statistically significant (HR = 4.08; 95{\%} CI = 1.56 to 10.71 comparing extreme BMI groups). More physical activity was related to lower all-cause 5-year mortality (HR = 0.57, 95{\%} CI = 0.33 to 0.98 for {\textgreater}7 hours/week vs never/rarely), but the association was attenuated after adjustment for BMI (HR = 0.64, 95{\%} CI = 0.37 to 1.12). No association was observed between physical activity and disease-specific mortality. Conclusions Our findings suggest that higher prediagnosis BMI increases risk of overall and disease-specific mortality among women diagnosed with endometrial cancer, whereas physical activity lowers risk. Intervention studies of the effect of these modifiable lifestyle factors on mortality are needed.},
author = {Arem, Hannah and Park, Yikyung and Pelser, Colleen and Ballard-Barbash, Rachel and Irwin, Melinda L. and Hollenbeck, Albert and Gierach, Gretchen L. and Brinton, Louise a. and Pfeiffer, Ruth M. and Matthews, Charles E.},
doi = {10.1093/jnci/djs530},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Arem et al. - 2013 - Prediagnosis body mass index, physical activity, and mortality in endometrial cancer patients.pdf:pdf},
isbn = {1460-2105 (Electronic)$\backslash$r0027-8874 (Linking)},
issn = {00278874},
journal = {J. Natl. Cancer Inst.},
number = {5},
pages = {342--349},
pmid = {23297041},
title = {{Prediagnosis body mass index, physical activity, and mortality in endometrial cancer patients}},
volume = {105},
year = {2013}
}
@article{Bell2005,
author = {Bell, Christopher G. and Walley, Andrew J. and Froguel, Phillipe},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Bell, Walley, Froguel - 2005 - The genetics of human obesity.pdf:pdf},
journal = {Nat. Rev. Genet.},
keywords = {obesity},
mendeley-tags = {obesity},
pages = {221--234},
title = {{The genetics of human obesity}},
volume = {6},
year = {2005}
}
@article{Stephens2011,
abstract = {Cancer is driven by somatically acquired point mutations and chromosomal rearrangements, conventionally thought to accumulate gradually over time. Using next-generation sequencing, we characterize a phenomenon, which we term chromothripsis, whereby tens to hundreds of genomic rearrangements occur in a one-off cellular crisis. Rearrangements involving one or a few chromosomes crisscross back and forth across involved regions, generating frequent oscillations between two copy number states. These genomic hallmarks are highly improbable if rearrangements accumulate over time and instead imply that nearly all occur during a single cellular catastrophe. The stamp of chromothripsis can be seen in at least 2{\%}-3{\%} of all cancers, across many subtypes, and is present in ???25{\%} of bone cancers. We find that one, or indeed more than one, cancer-causing lesion can emerge out of the genomic crisis. This phenomenon has important implications for the origins of genomic remodeling and temporal emergence of cancer. PaperClip: ?? 2011 Elsevier Inc.},
author = {Stephens, Philip J. and Greenman, Chris D. and Fu, Beiyuan and Yang, Fengtang and Bignell, Graham R. and Mudie, Laura J. and Pleasance, Erin D. and Lau, King Wai and Beare, David and Stebbings, Lucy A. and McLaren, Stuart and Lin, Meng Lay and McBride, David J. and Varela, Ignacio and Nik-Zainal, Serena and Leroy, Catherine and Jia, Mingming and Menzies, Andrew and Butler, Adam P. and Teague, Jon W. and Quail, Michael A. and Burton, John and Swerdlow, Harold and Carter, Nigel P. and Morsberger, Laura A. and Iacobuzio-Donahue, Christine and Follows, George A. and Green, Anthony R. and Flanagan, Adrienne M. and Stratton, Michael R. and Futreal, P. Andrew and Campbell, Peter J.},
doi = {10.1016/j.cell.2010.11.055},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Stephens et al.{\_}2011{\_}Massive genomic rearrangement acquired in a single catastrophic event during cancer development.pdf:pdf},
isbn = {1097-4172 (Electronic)$\backslash$r0092-8674 (Linking)},
issn = {00928674},
journal = {Cell},
keywords = {cancer,chromothripsis},
mendeley-tags = {cancer,chromothripsis},
number = {1},
pages = {27--40},
pmid = {21215367},
publisher = {Elsevier Inc.},
title = {{Massive genomic rearrangement acquired in a single catastrophic event during cancer development}},
volume = {144},
year = {2011}
}
@article{Zhang2011,
abstract = {The International Cancer Genome Consortium (ICGC) is a collaborative effort to characterize genomic abnormalities in 50 different cancer types. To make this data available, the ICGC has created the ICGC Data Portal. Powered by the BioMart software, the Data Portal allows each ICGC member institution to manage and maintain its own databases locally, while seamlessly presenting all the data in a single access point for users. The Data Portal currently contains data from 24 cancer projects, including ICGC, The Cancer Genome Atlas (TCGA), Johns Hopkins University, and the Tumor Sequencing Project. It consists of 3478 genomes and 13 cancer types and subtypes. Available open access data types include simple somatic mutations, copy number alterations, structural rearrangements, gene expression, microRNAs, DNA methylation and exon junctions. Additionally, simple germline variations are available as controlled access data. The Data Portal uses a web-based graphical user interface (GUI) to offer researchers multiple ways to quickly and easily search and analyze the available data. The web interface can assist in constructing complicated queries across multiple data sets. Several application programming interfaces are also available for programmatic access. Here we describe the organization, functionality, and capabilities of the ICGC Data Portal.},
author = {Zhang, Junjun and Baran, Joachim and Cros, A. and Guberman, Jonathan M. and Haider, Syed and Hsu, Jack and Liang, Yong and Rivkin, Elena and Wang, Jianxin and Whitty, Brett and Wong-Erasmus, Marie and Yao, Long and Kasprzyk, Arek},
doi = {10.1093/database/bar026},
file = {:Users/rikutakei/Downloads/papers/bar026.pdf:pdf},
isbn = {1758-0463 (Linking)},
issn = {17580463},
journal = {Database},
pages = {1--10},
pmid = {21930502},
title = {{International cancer genome consortium data portal-a one-stop shop for cancer genomics data}},
volume = {2011},
year = {2011}
}
@article{Print2016,
abstract = {BACKGROUND$\backslash$nMolecular markers have transformed our understanding of the heterogeneity of breast cancer, and have allowed the identification of genomic profiles of oestrogen receptor (ER)-$\alpha$ signalling. However, our understanding of the transcriptional profiles of ER signalling remains inadequate. Therefore, we aim to identify genomic indicators of ER pathway activity that could supplement traditional immunohistochemical (IHC) assessment of ER status, to better understand ER signalling in the breast tumours of individual patients. $\backslash$n$\backslash$nMETHODS$\backslash$nWe reduced ESR1 (gene encoding the ER-$\alpha$ protein) mRNA levels using siRNA in ER+ MCF7 breast cancer cells, and assayed for transcriptional changes using Affymetrix HG U133 Plus 2.0 arrays. We also compared 1034 ER+ and ER- breast tumours from publicly available microarray data. Principal components of ER activity generated from these analyses, and from other published oestrogen signatures, were compared with ESR1 expression, ER-$\alpha$ IHC, and patient survival. $\backslash$n$\backslash$nRESULTS$\backslash$nGenes differentially expressed in both analyses above were associated with ER-$\alpha$ IHC and ESR1 mRNA expression. They were also significantly enriched for oestrogen-driven molecular pathways associated with ESR1, CCND1, MYC and NFKB. Despite their differing constituent genes principal components generated from these new analyses, and from previously published ER-associated gene lists, were all associated and with the survival of breast cancer patients treated with endocrine therapies. $\backslash$n$\backslash$nCONCLUSION$\backslash$nA biomarker of ER-$\alpha$ pathway activity, generated using ESR1 responsive mRNAs in MCF7 cells, when used alongside ER-$\alpha$ IHC and ESR1 mRNA expression, may provide means for further stratification of patients and added insight into ER pathway activity in these patients.},
author = {Muthukaruppan, Anita and Lasham, Annette and Woad, Kathryn J. and Black, Michael A. and Blenkiron, Cherie and Miller, Lance D. and Harris, Gavin and McCarthy, Nicole and Findlay, Michael P. and Shelling, Andrew N. and Print, Cristin G.},
doi = {10.1016/j.clbc.2016.09.001},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Muthukaruppan et al. - 2016 - Multimodal assessment of oestrogen receptor mRNA profiles to quantify oestrogen pathway activity in breast.pdf:pdf},
issn = {15268209},
journal = {Clin. Breast Cancer},
keywords = {breast cancer,er,esr1,fi liated with school,gene expression,j,k,leicestershire,loughborough,mcf7,of veterinary medicine and,principal component analysis,rna,science,sutton bonington campus,university of nottingham,woad is currently af},
pages = {1--15},
publisher = {Elsevier Inc.},
title = {{Multimodal assessment of oestrogen receptor mRNA profiles to quantify oestrogen pathway activity in breast tumours}},
year = {2016}
}
@article{Metzker2010,
abstract = {Demand has never been greater for revolutionary technologies that deliver fast, inexpensive and accurate genome information. This challenge has catalysed the development of next-generation sequencing (NGS) technologies. The inexpensive production of large volumes of sequence data is the primary advantage over conventional methods. Here, I present a technical review of template preparation, sequencing and imaging, genome alignment and assembly approaches, and recent advances in current and near-term commercially available NGS instruments. I also outline the broad range of applications for NGS technologies, in addition to providing guidelines for platform selection to address biological questions of interest.},
archivePrefix = {arXiv},
arxivId = {209},
author = {Metzker, Michael L},
doi = {10.1038/nrg2626},
eprint = {209},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Metzker - 2010 - Sequencing technologies - the next generation.pdf:pdf},
isbn = {1471-0056},
issn = {1471-0056},
journal = {Nat. Rev. Genet.},
number = {1},
pages = {31--46},
pmid = {19997069},
publisher = {Nature Publishing Group},
title = {{Sequencing technologies - the next generation.}},
volume = {11},
year = {2010}
}
@article{Creighton2012,
abstract = {Obesity is thought to contribute to worse disease outcome in breast cancer as a result of increased levels of adipocyte-secreted endocrine factors, insulin, and insulin-like growth factors (IGFs) that accelerate tumor cell proliferation and impair treatment response. We examined the effects of patient obesity on primary breast tumor gene expression, by profiling transcription of a set of 103 tumors for which the patients' body mass index (BMI) was ascertained. Sample profiles were stratified according to patients' obesity phenotype defined as normal (BMI {\textless} 25), overweight (BMI 25-29.9), or obese (BMI ≥ 30). Widespread gene expression alterations were evident in breast tumors from obese patients as compared to other tumors, allowing us to define an obesity-associated cancer transcriptional signature of 662 genes. In multiple public expression data sets of breast cancers (representing {\textgreater} 1,500 patients), manifestation of the obesity signature patterns correlated with manifestation of a gene signature for IGF signaling and (to a lesser extent) with lower levels of estrogen receptor. In one patient cohort, manifestation of the obesity signature correlated with shorter time to metastases. A number of small molecules either induced or suppressed the obesity-associated transcriptional program in vitro; estrogens alpha-estradiol, levonorgestrel, and hexestrol induced the program, while several anti-parkinsonian agents targeting neurotransmitter receptor pathways repressed the program. Obesity in breast cancer patients appears to impact the gene expression patterns of the tumor (perhaps as a result of altered body chemistry). These results warrant further investigation of obesity-associated modifiers of breast cancer risk and disease outcome.},
author = {Creighton, Chad J. and Sada, Yvonne H. and Zhang, Yiqun and Tsimelzon, Anna and Wong, Helen and Dave, Bhuvanesh and Landis, Melissa D. and Bear, Harry D. and Rodriguez, Angel and Chang, Jenny C.},
doi = {10.1007/s10549-011-1595-y},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Creighton et al.{\_}2012{\_}A gene transcription signature of obesity in breast cancer.pdf:pdf},
isbn = {1573-7217 (Electronic) 0167-6806 (Linking)},
issn = {01676806},
journal = {Breast Cancer Res. Treat.},
keywords = {BMI,Breast cancer,Gene expression profiling,IGF,Insulin-like growth factor,Key Paper,Obesity},
mendeley-tags = {Key Paper},
pages = {993--1000},
pmid = {21750966},
title = {{A gene transcription signature of obesity in breast cancer}},
volume = {132},
year = {2012}
}
@article{Frese2007,
abstract = {Animal models of cancer provide an alternative means to determine the causes of and treatments for malignancy, thus representing a resource of immense potential for cancer medicine. The sophistication of modelling cancer in mice has increased to the extent that investigators can both observe and manipulate a complex disease process in a manner impossible to perform in patients. However, owing to limitations in model design and technology development, and the surprising underuse of existing models, only now are we realising the full potential of mouse models of cancer and what new approaches are needed to derive the maximum value for cancer patients from this investment.},
author = {Frese, Kristopher K and Tuveson, David a},
doi = {10.1038/nrc2192},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Frese, Tuveson - 2007 - Maximizing mouse cancer models.pdf:pdf},
isbn = {1474-175X 1474-1768},
issn = {1474-175X},
journal = {Nat. Rev. Cancer},
number = {9},
pages = {645--658},
pmid = {17687385},
title = {{Maximizing mouse cancer models}},
volume = {7},
year = {2007}
}
@article{Lagergren1999,
author = {Lagergren, Jesper},
doi = {10.7326/0003-4819-130-11-199906010-00003},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Lagergren{\_}1999{\_}Association between Body Mass and Adenocarcinoma of the Esophagus and Gastric Cardia.pdf:pdf},
issn = {0003-4819},
journal = {Ann. Intern. Med.},
month = {jun},
number = {11},
pages = {883--890},
publisher = {American College of Physicians},
title = {{Association between Body Mass and Adenocarcinoma of the Esophagus and Gastric Cardia}},
volume = {130},
year = {1999}
}
@article{Ferrara2009,
abstract = {Vascular endothelial growth factor (VEGF, VEGF-A) is a major regulator of physiological and pathological angiogenesis. Several VEGF inhibitors have been approved by the FDA for the treatment of advanced cancer and neovascular age-related macular degeneration. This brief review provides a historic account of the challenges associated with the discovery of VEGF and the early steps in elucidating the role of this molecule in the regulation of angiogenesis.},
archivePrefix = {arXiv},
arxivId = {arXiv:1011.1669v3},
author = {Ferrara, Napoleone},
doi = {10.1161/ATVBAHA.108.179663},
eprint = {arXiv:1011.1669v3},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Ferrara - 2009 - Vascular endothelial growth factor.pdf:pdf},
isbn = {1524-4636 (Electronic) 1079-5642 (Linking)},
issn = {10795642},
journal = {Arterioscler. Thromb. Vasc. Biol.},
keywords = {VEGF,angiogenesis,cancer},
mendeley-tags = {VEGF,angiogenesis,cancer},
number = {6},
pages = {789--791},
pmid = {19164810},
title = {{Vascular endothelial growth factor}},
volume = {29},
year = {2009}
}
@article{Johnson2007,
abstract = {Non-biological experimental variation or "batch effects" are commonly observed across multiple batches of microarray experiments, often rendering the task of combining data from these batches difficult. The ability to combine microarray data sets is advantageous to researchers to increase statistical power to detect biological phenomena from studies where logistical considerations restrict sample size or in studies that require the sequential hybridization of arrays. In general, it is inappropriate to combine data sets without adjusting for batch effects. Methods have been proposed to filter batch effects from data, but these are often complicated and require large batch sizes ( {\textgreater} 25) to implement. Because the majority of microarray studies are conducted using much smaller sample sizes, existing methods are not sufficient. We propose parametric and non-parametric empirical Bayes frameworks for adjusting data for batch effects that is robust to outliers in small sample sizes and performs comparable to existing methods for large samples. We illustrate our methods using two example data sets and show that our methods are justifiable, easy to apply, and useful in practice. Software for our method is freely available at: http://biosun1.harvard.edu/complab/batch/.},
author = {Johnson, W. Evan and Li, Cheng and Rabinovic, Ariel},
doi = {10.1093/biostatistics/kxj037},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Johnson, Li, Rabinovic - 2007 - Adjusting batch effects in microarray expression data using empirical Bayes methods.pdf:pdf},
isbn = {1465-4644, 1468-4357},
issn = {14654644},
journal = {Biostatistics},
keywords = {Batch effects,Empirical Bayes,Microarrays,Monte Carlo},
number = {1},
pages = {118--127},
pmid = {16632515},
title = {{Adjusting batch effects in microarray expression data using empirical Bayes methods}},
volume = {8},
year = {2007}
}
@article{Perera1997,
abstract = {Acting in concert with individual susceptibility, environmental factors such as smoking, diet, and pollutants play a role in most human cancer. However, new molecular evidence indicates that specific groups-characterized by predisposing genetic traits or ethnicity, the very young, and women-may have heightened risk from certain exposures. This is illustrated by molecular epidemiologic studies of environmental carcinogens such as polycyclic aromatic hydrocarbons and aromatic amines. Individual genetic screening for rare high-risk traits or for more common, low-penetrant susceptibility genes is problematic and not routinely recommended. However, knowledge of the full spectrum of both genetic and acquired susceptibility in the population will be instrumental in developing health and regulatory policies that increase protection of the more susceptible groups from risks of environmental carcinogens. This will necessitate revision of current risk assessment methodologies to explicitly account for individual variation in susceptibility to environmental carcinogens.},
author = {Perera, F P},
doi = {10.1126/science.278.5340.1068},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Perera - 1997 - Environment and cancer who are susceptible.pdf:pdf},
isbn = {00368075$\backslash$r10959203},
issn = {00368075},
journal = {Science (80-. ).},
keywords = {environmental factors,lung cancer,tobacco},
mendeley-tags = {environmental factors,lung cancer,tobacco},
number = {5340},
pages = {1068--1073},
pmid = {9353182},
title = {{Environment and cancer: who are susceptible?}},
volume = {278},
year = {1997}
}
@article{Bernstein1993,
abstract = {There is substantial evidence that high estrogen levels in postmenopausal women are associated with an increase in breast cancer risk, but such a relation has not yet been established in premenopausal women, despite biologic evidence that breast epithelial cell division rates are high during the luteal phase of the menstrual cycle when estradiol and progesterone levels are high. The lack of total consistency among studies that have assessed estrogen differences, whether in breast cancer patients versus controls or in subgroups of the population characterized by different risk profiles for breast cancer, is not unexpected given the extraordinarily complex methodological issues that must be addressed in these studies. There has been a clear evolution over time in the level of sophistication of these types of studies, further decreasing the likelihood of finding consistent patterns in the literature. Other hormones may play an important role in breast cancer development as well. Experimental data are particularly compelling for a role of progesterone and prolactin, but hormonal studies in women are not entirely convincing regarding the role of these two hormones, nor is the literature nearly as extensive as it is for the estrogens. Studies of various androgens are even less consistent. Moreover, such studies suffer from a lack of precise hypotheses regarding how these hormones might directly alter risk.},
author = {Bernstein, L and Ross, R K},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Bernstein, Ross{\_}1993{\_}Endogenous hormones and breast cancer risk.pdf:pdf},
isbn = {0193-936X (Print)$\backslash$r0193-936X (Linking)},
issn = {0193-936X},
journal = {Epidemiol. Rev.},
number = {1},
pages = {48--65},
pmid = {8405212},
title = {{Endogenous hormones and breast cancer risk.}},
volume = {15},
year = {1993}
}
@article{Chen1996,
abstract = {OB-R is a high affinity receptor for leptin, an important circulating signal for the regulation of body weight. We identified an alternatively spliced transcript that encodes a form of mouse OB-R with a long intracellular domain. db/db mice also produce this alternatively spliced transcript, but with a 106 nt insertion that prematurely terminates the intracellular domain. We further identified a G???T point mutation in the genomic OB-R sequence in db/db mice. This mutation generates a donor splice site that converts the 106 nt region to a novel exon retained in the OB-R transcript. We predict that the long intracellular domain form of OB-R is crucial for initiating intracellular signal transduction, and as a corollary, the inability to produce this form of OB-R leads to the severe obese phenotype found in db/db mice.},
author = {Chen, Hong and Charlat, Olga and Tartaglia, Louis A. and Woolf, Elizabeth A. and Weng, Xun and Ellis, Stephen J. and Lakey, Nathan D. and Culpepper, Janice and More, Karen J. and Breitbart, Roger E. and Duyk, Geoffrey M. and Tepper, Robert I. and Morgenstern, Jay P.},
doi = {10.1016/S0092-8674(00)81294-5},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Chen et al. - 1996 - Evidence that the diabetes gene encodes the leptin receptor Identification of a mutation in the leptin receptor gen.pdf:pdf},
isbn = {0092-8674 (Print)$\backslash$r0092-8674 (Linking)},
issn = {00928674},
journal = {Cell},
keywords = {leptin},
mendeley-tags = {leptin},
number = {3},
pages = {491--495},
pmid = {8608603},
title = {{Evidence that the diabetes gene encodes the leptin receptor: Identification of a mutation in the leptin receptor gene in db/db mice}},
volume = {84},
year = {1996}
}
@misc{TCGA,
author = {{National Cancer Institute} and {National Human Genome Research Institute}},
title = {{The Cancer Genome Atlas}},
url = {https://cancergenome.nih.gov/},
urldate = {2015-04-01},
year = {2016}
}
@article{Spanswick1997,
abstract = {Leptin, the protein encoded by the obese (ob) gene, is secreted from adipose tissue and is thought to act in the central nervous system to regulate food intake and body weight. It has been proposed that leptin acts in the hypothalamus, the main control centre for satiety and energy expenditure. Mutations in leptin or the receptor isoform (Ob-R[L]) present in hypothalamic neurons result in profound obesity and symptoms of non-insulin-dependent diabetes. Here we show that leptin hyperpolarizes glucose-receptive hypothalamic neurons of lean Sprague-Dawley and Zucker rats, but is ineffective on neurons of obese Zucker (fa/fa) rats. This hyperpolarization is due to the activation of a potassium current, and is not easily recovered on removal of leptin, but is reversed by applying the sulphonylurea, tolbutamide. Single-channel recordings demonstrate that leptin activates an ATP-sensitive potassium (K[ATP]) channel. Our data indicate that the K(ATP) channel may function as the molecular end-point of the pathway following leptin activation of the Ob-R(L) receptor in hypothalamic neurons.},
author = {Spanswick, D and Smith, M a and Groppi, V E and Logan, S D and Ashford, M L},
doi = {10.1038/37379},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Spanswick et al. - 1997 - Leptin inhibits hypothalamic neurons by activation of ATP-sensitive potassium channels.pdf:pdf},
isbn = {0028-0836 (Print)$\backslash$r0028-0836},
issn = {0028-0836},
journal = {Nature},
keywords = {insulin,leptin},
mendeley-tags = {insulin,leptin},
number = {6659},
pages = {521--525},
pmid = {9394003},
title = {{Leptin inhibits hypothalamic neurons by activation of ATP-sensitive potassium channels.}},
volume = {390},
year = {1997}
}
@article{Kearney2010,
abstract = {A picture of food consumption (availability) trends and projections to 2050, both globally and for different regions of the world, along with the drivers largely responsible for these observed consumption trends are the subject of this review. Throughout the world, major shifts in dietary patterns are occurring, even in the consumption of basic staples towards more diversified diets. Accompanying these changes in food consumption at a global and regional level have been considerable health consequences. Populations in those countries undergoing rapid transition are experiencing nutritional transition. The diverse nature of this transition may be the result of differences in socio-demographic factors and other consumer characteristics. Among other factors including urbanization and food industry marketing, the policies of trade liberalization over the past two decades have implications for health by virtue of being a factor in facilitating the 'nutrition transition' that is associated with rising rates of obesity and chronic diseases such as cardiovascular disease and cancer. Future food policies must consider both agricultural and health sectors, thereby enabling the development of coherent and sustainable policies that will ultimately benefit agriculture, human health and the environment.},
author = {Kearney, John},
doi = {10.1098/rstb.2010.0149},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Kearney - 2010 - Food consumption trends and drivers.pdf:pdf},
isbn = {1471-2970 (Electronic)$\backslash$r0962-8436 (Linking)},
issn = {0962-8436},
journal = {Philos. Trans. R. Soc. B Biol. Sci.},
keywords = {Agriculture,Food Supply,Humans,Nutrition Policy,Nutritional Status,obesity},
mendeley-tags = {obesity},
number = {1554},
pages = {2793--2807},
pmid = {20713385},
title = {{Food consumption trends and drivers}},
volume = {365},
year = {2010}
}
@article{Buchwald2004,
abstract = {Bariatric surgery is currently the only effective long-term treatment of morbid obesity and its related co-morbidities. Gastric bypass, adjustable gastric banding, and duodenal switch with biliopancreatic diversion are the three most common operations performed in the United States to induce sustained weight loss. Patient selection is important since compliance postoperatively leads to a successful outcome in over 80{\%} of patients. Preoperative psychological and behavioral problems may lead to maladaptive eating habits postoperatively that defeat the purpose of the surgery. To date, we do not have a 100{\%} reliable method of profiling patients who will fail to keep weight off for the long term. It is therefore important that patients who have preoperative psychological problems that may lead to failure to lose or keep weight off after surgery are offered postoperative counseling along with group support},
author = {Buchwald, Henry and Avidor, Yoav and Braunwald, Eugene and Jensen, Michael D. and Pories, Walter and Fahrbach, Kyle and Schoelles, Karen},
doi = {10.1016/j.clindermatol.2004.01.007},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Buchwald et al. - 2004 - Bariatric surgery a systematic review and meta-analysis.pdf:pdf},
isbn = {1743-9159 (Electronic)$\backslash$n1743-9159 (Linking)},
issn = {0738081X},
journal = {JAMA},
keywords = {Article,Bariatric surgery,Biliopancreatic Diversion,Comorbidity,Compliance,Counseling,Eating,Gastric Bypass,Habits,Medicine,Morbid obesity,Obesity,Patient Selection,Patients,Universities,Weight Loss,obesity,surgery,treatment,united states},
mendeley-tags = {obesity},
pages = {1724--1737},
pmid = {16418542},
title = {{Bariatric surgery: a systematic review and meta-analysis}},
volume = {292},
year = {2004}
}
@article{Hurd2009,
abstract = {Several recent studies from the field of epigenetics have combined chromatin-immunoprecipitation (ChIP) with next-generation high-throughput sequencing technologies to describe the locations of histone post-translational modifications (PTM) and DNA methylation genome-wide. While these reports begin to quench the chromatin biologists thirst for visualizing where in the genome epigenetic marks are placed, they also illustrate several advantages of sequencing based genomics compared to microarray analysis. Accordingly, next-generation sequencing (NGS) technologies are now challenging microarrays as the tool of choice for genome analysis. The increased affordability of comprehensive sequence-based genomic analysis will enable new questions to be addressed in many areas of biology. It is inevitable that massively-parallel sequencing platforms will supercede the microarray for many applications, however, there are niches for microarrays to fill and interestingly we may very well witness a symbiotic relationship between microarrays and high-throughput sequencing in the future.},
author = {Hurd, Paul J. and Nelson, Christopher J.},
doi = {10.1093/bfgp/elp013},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Hurd, Nelson - 2009 - Advantages of next-generation sequencing versus the microarray in epigenetic research.pdf:pdf},
isbn = {1477-4062 (Electronic)$\backslash$r1473-9550 (Linking)},
issn = {14739550},
journal = {Briefings Funct. Genomics Proteomics},
keywords = {ABI SOLiD,ChIP-Seq,Microarray,Next-generation sequencing,Roche 454 pyrosequencing,Solexa/Illumina},
number = {3},
pages = {174--183},
pmid = {19535508},
title = {{Advantages of next-generation sequencing versus the microarray in epigenetic research}},
volume = {8},
year = {2009}
}
@article{Fuentes-Mattei2014,
abstract = {BACKGROUND: Obesity increases the risk of cancer death among postmenopausal women with estrogen receptor-positive (ER+) breast cancer, but the direct evidence for the mechanisms is lacking. The purpose of this study is to demonstrate direct evidence for the mechanisms mediating this epidemiologic phenomenon. METHODS: We analyzed transcriptomic profiles of pretreatment biopsies from a prospective cohort of 137 ER+ breast cancer patients. We generated transgenic (MMTV-TGF$\alpha$;A (y) /a) and orthotopic/syngeneic (A (y) /a) obese mouse models to investigate the effect of obesity on tumorigenesis and tumor progression and to determine biological mechanisms using whole-genome transcriptome microarrays and protein analyses. We used a coculture system to examine the impact of adipocytes/adipokines on breast cancer cell proliferation. All statistical tests were two-sided. RESULTS: Functional transcriptomic analysis of patients revealed the association of obesity with 59 biological functional changes (P {\textless} .05) linked to cancer hallmarks. Gene enrichment analysis revealed enrichment of AKT-target genes (P = .04) and epithelial-mesenchymal transition genes (P = .03) in patients. Our obese mouse models demonstrated activation of the AKT/mTOR pathway in obesity-accelerated mammary tumor growth (3.7- to 7.0-fold; P {\textless} .001; n = 6-7 mice per group). Metformin or everolimus can suppress obesity-induced secretion of adipokines and breast tumor formation and growth (0.5-fold, P = .04; 0.3-fold, P {\textless} .001, respectively; n = 6-8 mice per group). The coculture model revealed that adipocyte-secreted adipokines (eg, TIMP-1) regulate adipocyte-induced breast cancer cell proliferation and invasion. Metformin suppress adipocyte-induced cell proliferation and adipocyte-secreted adipokines in vitro. CONCLUSIONS: Adipokine secretion and AKT/mTOR activation play important roles in obesity-accelerated breast cancer aggressiveness in addition to hyperinsulinemia, estrogen signaling, and inflammation. Metformin and everolimus have potential for therapeutic interventions of ER+ breast cancer patients with obesity.},
author = {Fuentes-Mattei, Enrique and Velazquez-Torres, Guermarie and Phan, Liem and Zhang, F. and Chou, P.-C. and Shin, J.-H. and Choi, Hyun Ho and Chen, J.-S. and Zhao, Ruiying and Chen, Jian and Gully, Chris and Carlock, Colin and Qi, Yuan and Zhang, Ya and Wu, Yun and Esteva, Francisco J. and Luo, Yongde and McKeehan, Wallace L. and Ensor, Joe and Hortobagyi, Gabriel N. and Pusztai, Lajos and {Fraser Symmans}, W. and Lee, M.-H. and {Jim Yeung}, S.-C.},
doi = {10.1093/jnci/dju158},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Fuentes-Mattei et al.{\_}2014{\_}Effects of Obesity on Transcriptomic Changes and Cancer Hallmarks in Estrogen Receptor-Positive Breast Cancer.pdf:pdf},
issn = {0027-8874},
journal = {J. Natl. Cancer Inst.},
keywords = {Key Paper},
mendeley-tags = {Key Paper},
month = {jun},
number = {7},
pages = {dju158},
pmid = {24957076},
title = {{Effects of Obesity on Transcriptomic Changes and Cancer Hallmarks in Estrogen Receptor-Positive Breast Cancer}},
volume = {106},
year = {2014}
}
@article{Renan1993,
author = {Renan, M. J.},
doi = {10.1002/mc.2940070303},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Renan - 1993 - How many mutations are required for tumorigenesis Implications from human cancer data.pdf:pdf},
isbn = {0899-1987 (Print)$\backslash$r0899-1987 (Linking)},
issn = {08991987},
journal = {Mol. Carcinog.},
keywords = {cancer},
mendeley-tags = {cancer},
number = {3},
pages = {139--146},
pmid = {8489711},
title = {{How many mutations are required for tumorigenesis? Implications from human cancer data}},
volume = {7},
year = {1993}
}
@article{Yancopoulos2000,
author = {Yancopoulos, George D and Gale, Nicholas W and Davis, Samuel and Gale, Nicholas W and Rudge, John S and Wiegand, Stanley J and Holash, Jocelyn},
doi = {10.1038/35025215},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Yancopoulos et al. - 2000 - Vascular-Specific Growth Factors and Blood Vessel Formation.pdf:pdf},
journal = {Nature},
keywords = {angiogenesis,cancer},
mendeley-tags = {angiogenesis,cancer},
pages = {242--248},
title = {{Vascular-Specific Growth Factors and Blood Vessel Formation}},
volume = {407},
year = {2000}
}
@article{Freedman2001,
abstract = {BACKGROUND: Childhood obesity is related to adult levels of lipids, lipoproteins, blood pressure, and insulin and to morbidity from coronary heart disease (CHD). However, the importance of the age at which obesity develops in these associations remains uncertain. OBJECTIVE AND DESIGN: We assessed the longitudinal relationship of childhood body mass index (BMI, kg/m(2)) to adult levels of lipids, insulin, and blood pressure among 2617 participants. All participants were initially examined at ages 2 to 17 years and were reexamined at ages 18 to 37 years; the mean follow-up was 17 years. RESULTS: Of the overweight children (BMI {\textgreater}/=95th percentile), 77{\%} remained obese ({\textgreater}/=30 kg/m(2)) as adults. Childhood overweight was related to adverse risk factor levels among adults, but associations were weak (r {\~{}} 0.1-0.3) and were attributable to the strong persistence of weight status between childhood and adulthood. Although obese adults had adverse levels of lipids, insulin, and blood pressure, levels of these risk factors did not vary with childhood weight status or with the age ({\textless}/=8 years, 12-17 years, or {\textgreater}/=18 years) of obesity onset. CONCLUSIONS: Additional data are needed to assess the independent relationship of childhood weight status to CHD morbidity. Because normal-weight children who become obese adults have adverse risk factor levels and probably will be at increased risk for adult morbidity, our results emphasize the need for both primary and secondary prevention.},
author = {Freedman, DS and Khan, LK and Dietz, WH and Srinivasan, SR and Berenson, GS},
doi = {10.1542/peds.108.3.712},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Freedman et al. - 2001 - Relationship of childhood obesity to coronary heart disease risk factors in adulthood the Bogalusa Heart Study.pdf:pdf},
isbn = {1098-4275},
issn = {1098-4275 (Electronic)},
journal = {Pediatrics},
keywords = {obesity},
mendeley-tags = {obesity},
number = {3},
pages = {712--718},
pmid = {11533341},
title = {{Relationship of childhood obesity to coronary heart disease risk factors in adulthood: the Bogalusa Heart Study.}},
volume = {108},
year = {2001}
}
@article{Mani2008a,
abstract = {The epithelial-mesenchymal transition (EMT) is a key developmental program that is often activated during cancer invasion and metastasis. We here report that the induction of an EMT in immortalized human mammary epithelial cells (HMLEs) results in the acquisition of mesenchymal traits and in the expression of stem-cell markers. Furthermore, we show that those cells have an increased ability to form mammospheres, a property associated with mammary epithelial stem cells. Independent of this, stem cell-like cells isolated from HMLE cultures form mammospheres and express markers similar to those of HMLEs that have undergone an EMT. Moreover, stem-like cells isolated either from mouse or human mammary glands or mammary carcinomas express EMT markers. Finally, transformed human mammary epithelial cells that have undergone an EMT form mammospheres, soft agar colonies, and tumors more efficiently. These findings illustrate a direct link between the EMT and the gain of epithelial stem cell properties. ?? 2008 Elsevier Inc. All rights reserved.},
author = {Mani, Sendurai A. and Guo, Wenjun and Liao, Mai Jing and Eaton, Elinor Ng and Ayyanan, Ayyakkannu and Zhou, Alicia Y. and Brooks, Mary and Reinhard, Ferenc and Zhang, Cheng Cheng and Shipitsin, Michail and Campbell, Lauren L. and Polyak, Kornelia and Brisken, Cathrin and Yang, Jing and Weinberg, Robert A.},
doi = {10.1016/j.cell.2008.03.027},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Mani et al. - 2008 - The Epithelial-Mesenchymal Transition Generates Cells with Properties of Stem Cells.pdf:pdf},
isbn = {0092-8674},
issn = {00928674},
journal = {Cell},
keywords = {CELLBIO,EMT,HUMDISEASE,STEMCELL,cancer,metastasis},
mendeley-tags = {EMT,cancer,metastasis},
number = {4},
pages = {704--715},
pmid = {18485877},
title = {{The Epithelial-Mesenchymal Transition Generates Cells with Properties of Stem Cells}},
volume = {133},
year = {2008}
}
@article{Adams2007,
abstract = {Impaired apoptosis is both critical in cancer development and a major barrier to effective treatment. In response to diverse intracellular damage signals, including those evoked by cancer therapy, the cell's decision to undergo apoptosis is determined by interactions between three factions of the Bcl-2 protein family. The damage signals are transduced by the diverse 'BH3-only' proteins, distinguished by the BH3 domain used to engage their pro-survival relatives: Bcl-2, Bcl-x(L), Bcl-w, Mcl-1 and A1. This interaction ablates pro-survival function and allows activation of Bax and Bak, which commit the cell to apoptosis by permeabilizing the outer membrane of the mitochondrion. Certain BH3-only proteins (e.g. Bim, Puma) can engage all the pro-survival proteins, but others (e.g. Bad, Noxa) engage only subsets. Activation of Bax and Bak appears to require that the BH3-only proteins engage the multiple pro-survival proteins guarding Bax and Bak, rather than binding to the latter. The balance between the pro-survival proteins and their BH3 ligands regulates tissue homeostasis, and either overexpression of a pro-survival family member or loss of a proapoptotic relative can be oncogenic. Better understanding of the Bcl-2 family is clarifying its role in cancer development, revealing how conventional therapy works and stimulating the search for "BH3 mimetics" as a novel class of anticancer drugs.},
author = {Adams, J M and Cory, S},
doi = {10.1038/sj.onc.1210220},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Adams, Cory - 2007 - The Bcl-2 apoptotic switch in cancer development and therapy.pdf:pdf},
isbn = {0950-9232},
issn = {0950-9232},
journal = {Oncogene},
keywords = {Apoptosis,Apoptosis: physiology,Humans,Molecular Mimicry,Neoplasms,Neoplasms: pathology,Neoplasms: physiopathology,Neoplasms: therapy,Proto-Oncogene Proteins c-bcl-2,Proto-Oncogene Proteins c-bcl-2: physiology},
number = {9},
pages = {1324--1337},
pmid = {17322918},
title = {{The Bcl-2 apoptotic switch in cancer development and therapy.}},
volume = {26},
year = {2007}
}
@article{Yu2014,
author = {Yu, Hua and Lee, Heehyoung and Herrmann, Andreas and Buettner, Ralf and Jove, Richard},
doi = {10.1038/nrc3818},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Yu et al. - 2014 - Revisiting STAT3 signalling in cancer new and unexpected biological functions.pdf:pdf},
issn = {1474-175X},
journal = {Nat. Rev. Cancer},
keywords = {cancer,inflammation},
mendeley-tags = {cancer,inflammation},
number = {11},
pages = {736--746},
publisher = {Nature Publishing Group},
title = {{Revisiting STAT3 signalling in cancer : new and unexpected biological functions}},
volume = {14},
year = {2014}
}
@article{Osborne2011,
abstract = {The estrogen receptor (ER) pathway plays a pivotal role in breast cancer development and progression. Endocrine therapy to block the ER pathway is highly effective, but its usefulness is limited by common intrinsic and acquired resistance. Multiple mechanisms responsible for endocrine resistance have been proposed and include deregulation of various components of the ER pathway itself, alterations in cell cycle and cell survival signaling molecules, and the activation of escape pathways that can provide tumors with alternative proliferative and survival stimuli. Among these, increased expression or signaling of growth factor receptor pathways, especially the EGFR/HER2 pathway, has been associated with both experimental and clinical endocrine therapy resistance. New treatment combinations targeting both ER and growth factor receptor signaling to block the crosstalk between these pathways and eliminate escape routes have been proven highly effective in preclinical models. Results of recent clinical studies, while partly supporting this approach, also highlight the need to better identify a priori the patients whose tumors are most likely to benefit from these specific cotargeting strategies.},
author = {Osborne, C Kent and Schiff, Rachel},
doi = {10.1146/annurev-med-070909-182917},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Osborne, Schiff{\_}2011{\_}Mechanisms of endocrine resistance in breast cancer.pdf:pdf},
isbn = {1545-326X (Electronic)$\backslash$r0066-4219 (Linking)},
issn = {0066-4219},
journal = {Annu. Rev. Med.},
keywords = {combination therapy,crosstalk,endocrine therapy,estrogen receptor,growth factor receptor,signaling},
pages = {233--247},
pmid = {20887199},
title = {{Mechanisms of endocrine resistance in breast cancer.}},
volume = {62},
year = {2011}
}
@article{Calle2003,
author = {Calle, Eugene E. and Rodriguez, Carmen and Walker-Thurmond, Kimberly and Thun, Michael J.},
doi = {10.1056/NEJMoa0810625)},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Calle et al. - 2003 - Overweight, obesity, and mortality from cancer in a prospectively studied cofort of U.S. adults.pdf:pdf},
journal = {N. Engl. J. Med.},
keywords = {obesity},
mendeley-tags = {obesity},
number = {17},
pages = {1625--1638},
title = {{Overweight, obesity, and mortality from cancer in a prospectively studied cofort of U.S. adults}},
volume = {348},
year = {2003}
}
@article{Talmadge2010,
abstract = {Metastasis resistant to therapy is the major cause of death from cancer. Despite almost 200 years of study, the process of tumor metastasis remains controversial. Stephen Paget initially identified the role of host-tumor interactions on the basis of a review of autopsy records. His "seed and soil" hypothesis was substantiated a century later with experimental studies, and numerous reports have confirmed these seminal observations. An improved understanding of the metastatic process and the attributes of the cells selected by this process is critical for the treatment of patients with systemic disease. In many patients, metastasis has occurred by the time of diagnosis, so metastasis prevention may not be relevant. Treating systemic disease and identifying patients with early disease should be our goal. Revitalized research in the past three decades has focused on new discoveries in the biology of metastasis. Even though our understanding of molecular events that regulate metastasis has improved, the contributions and timing of molecular lesion(s) involved in metastasis pathogenesis remain unclear. Review of the history of pioneering observations and discussion of current controversies should increase understanding of the complex and multifactorial interactions between the host and selected tumor cells that contribute to fatal metastasis and should lead to the design of successful therapy.},
archivePrefix = {arXiv},
arxivId = {NIHMS150003},
author = {Talmadge, James E. and Fidler, Isaiah J.},
doi = {10.1158/0008-5472.CAN-10-1040},
eprint = {NIHMS150003},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Talmadge, Fidler - 2010 - AACR centennial series The biology of cancer metastasis Historical perspective.pdf:pdf},
isbn = {0008-5472},
issn = {00085472},
journal = {Cancer Res.},
keywords = {cancer,metastasis},
mendeley-tags = {cancer,metastasis},
number = {14},
pages = {5649--5669},
pmid = {20610625},
title = {{AACR centennial series: The biology of cancer metastasis: Historical perspective}},
volume = {70},
year = {2010}
}
@article{Yap2012,
abstract = {Most advanced solid tumors remain incurable, with resistance to chemotherapeutics and targeted therapies a common cause of poor clinical outcome. Intratumor heterogeneity may contribute to this failure by initiating phenotypic diversity enabling drug resistance to emerge and by introducing tumor sampling bias. Envisaging tumor growth as a Darwinian tree with the trunk representing ubiquitous mutations and the branches representing heterogeneous mutations may help in drug discovery and the development of predictive biomarkers of drug response.},
author = {Yap, T. A. and Gerlinger, M. and Futreal, P. A. and Pusztai, L. and Swanton, C.},
doi = {10.1126/scitranslmed.3003854},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Yap et al.{\_}2012{\_}Intratumor Heterogeneity Seeing the Wood for the Trees.pdf:pdf},
isbn = {1946-6242 (Electronic)$\backslash$n1946-6234 (Linking)},
issn = {1946-6234},
journal = {Sci. Transl. Med.},
number = {127},
pages = {127ps10--127ps10},
pmid = {22461637},
title = {{Intratumor Heterogeneity: Seeing the Wood for the Trees}},
volume = {4},
year = {2012}
}
@article{Barsh2002,
abstract = {The homeostatic regulation of adiposity is a physiological concept that originated nearly 70 years ago, the genetic foundations of which have just begun to emerge. A key element of this concept is the existence of one or more humoral mediators, which circulate at levels that reflect body fat stores and which signal through neuronal receptors to elicit appropriate behavioural and metabolic responses over short time periods. Initial insights into adiposity regulation came from the positional cloning of mouse obesity mutations, but the field is now poised to address specific physiological questions using more sophisticated genetic approaches.},
author = {Barsh, Gregory S and Schwartz, Michael W},
doi = {10.1038/nrg862},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Barsh, Schwartz - 2002 - Genetic approaches to studying energy balance perception and integration.pdf:pdf},
isbn = {1471-0056 (Print)$\backslash$n1471-0056 (Linking)},
issn = {1471-0056},
journal = {Nat. Rev. Genet.},
keywords = {Adipose Tissue,Adipose Tissue: metabolism,Animals,Biological,Brown,Brown: physiology,Energy Metabolism,Energy Metabolism: physiology,Humans,Models,Obesity,Obesity: etiology,Obesity: metabolism,Proteins,Proteins: genetics,Proteins: physiology,obesity},
mendeley-tags = {obesity},
number = {8},
pages = {589--600},
pmid = {12154382},
title = {{Genetic approaches to studying energy balance: perception and integration.}},
volume = {3},
year = {2002}
}
@article{Alter2000,
abstract = {We describe the use of singular value decomposition in transforming genome-wide expression data from genes x arrays space to reduced diagonalized "eigengenes" x "eigenarrays" space, where the eigengenes (or eigenarrays) are unique orthonormal superpositions of the genes (or arrays). Normalizing the data by filtering out the eigengenes (and eigenarrays) that are inferred to represent noise or experimental artifacts enables meaningful comparison of the expression of different genes across different arrays in different experiments. Sorting the data according to the eigengenes and eigenarrays gives a global picture of the dynamics of gene expression, in which individual genes and arrays appear to be classified into groups of similar regulation and function, or similar cellular state and biological phenotype, respectively. After normalization and sorting, the significant eigengenes and eigenarrays can be associated with observed genome-wide effects of regulators, or with measured samples, in which these regulators are overactive or underactive, respectively.},
author = {Alter, O. and Brown, P. O. and Botstein, D.},
doi = {10.1073/pnas.97.18.10101},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Alter, Brown, Botstein - 2000 - Singular value decomposition for genome-wide expression data processing and modeling.pdf:pdf},
isbn = {0027-8424},
issn = {0027-8424},
journal = {Proc. Natl. Acad. Sci.},
keywords = {Biological,Cell Cycle,Fungal,Genetic,Genome,Mathematics,Models,Oligonucleotide Array Sequence Analysis,Open Reading Frames,Saccharomyces cerevisiae,Saccharomyces cerevisiae: cytology,Saccharomyces cerevisiae: genetics,Statistical},
number = {18},
pages = {10101--10106},
pmid = {10963673},
title = {{Singular value decomposition for genome-wide expression data processing and modeling}},
volume = {97},
year = {2000}
}
@article{VanHubbardS2000,
author = {{Van Hubbard S}},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Van Hubbard S - 2000 - Defining overweight and obesity what are the issues.pdf:pdf},
journal = {Am J Clin Nutr},
keywords = {obesity},
mendeley-tags = {obesity},
pages = {1067--8},
title = {{Defining overweight and obesity: what are the issues}},
volume = {72},
year = {2000}
}
@article{Yu2007,
abstract = {Immune cells in the tumour microenvironment not only fail to mount an effective anti-tumour immune response, but also interact intimately with the transformed cells to promote oncogenesis actively. Signal transducer and activator of transcription 3 (STAT3), which is a point of convergence for numerous oncogenic signalling pathways, is constitutively activated both in tumour cells and in immune cells in the tumour microenvironment. Constitutively activated STAT3 inhibits the expression of mediators necessary for immune activation against tumour cells. Furthermore, STAT3 activity promotes the production of immunosuppressive factors that activate STAT3 in diverse immune-cell subsets, altering gene-expression programmes and, thereby, restraining anti-tumour immune responses. As such, STAT3 propagates several levels of crosstalk between tumour cells and their immunological microenvironment, leading to tumour-induced immunosuppression. Consequently, STAT3 has emerged as a promising target for cancer immunotherapy.},
author = {Yu, Hua and Kortylewski, Marcin and Pardoll, Drew},
doi = {10.1038/nri1995},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Yu, Kortylewski, Pardoll - 2007 - Crosstalk between cancer and immune cells role of STAT3 in the tumour microenvironment.pdf:pdf},
isbn = {1474-1733 (Print)$\backslash$r1474-1733 (Linking)},
issn = {1474-1733},
journal = {Nat. Rev. Immunol.},
keywords = {cancer,stat3},
mendeley-tags = {cancer,stat3},
number = {January},
pages = {41--51},
pmid = {17186030},
title = {{Crosstalk between cancer and immune cells: role of STAT3 in the tumour microenvironment}},
volume = {7},
year = {2007}
}
@article{Wardburg1956,
abstract = {Metastasis involves the spread of cancer cells from the primary tumor to surrounding tissues and to distant organs and is the primary cause of cancer morbidity and mortality. In order to complete the metastatic cascade, cancer cells must detach from the primary tumor, intravasate into the circulatory and lymphatic systems, evade immune attack, extravasate at distant capillary beds, and invade and proliferate in distant organs. Currently, several hypotheses have been advanced to explain the origin of cancer metastasis. These involve an epithelial mesenchymal transition, an accumulation of mutations in stem cells, a macrophage facilitation process, and a macrophage origin involving either transformation or fusion hybridization with neoplastic cells. Many of the properties of metastatic cancer cells are also seen in normal macrophages. A macrophage origin of metastasis can also explain the long-standing "seed and soil" hypothesis and the absence of metastasis in plant cancers. The view of metastasis as a macrophage metabolic disease can provide novel insight for therapeutic management.},
archivePrefix = {arXiv},
arxivId = {NIHMS150003},
author = {Wardburg, Otto},
doi = {10.1016/S0306-9877(96)90136-X},
eprint = {NIHMS150003},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Wardburg - 1956 - On the origin of cancer cells.pdf:pdf},
isbn = {9780199865093},
issn = {0893-9675},
journal = {Science (80-. ).},
keywords = {cancer},
mendeley-tags = {cancer},
number = {3191},
pages = {309--314},
pmid = {23237552},
title = {{On the origin of cancer cells}},
volume = {123},
year = {1956}
}
@article{Pikarsky2004,
abstract = {The causes of sporadic human cancer are seldom recognized, but it is estimated that carcinogen exposure and chronic inflammation are two important underlying conditions for tumour development, the latter accounting for approximately 20{\%} of human cancer. Whereas the causal relationship between carcinogen exposure and cancer has been intensely investigated, the molecular and cellular mechanisms linking chronic inflammation to tumorigenesis remain largely unresolved. We proposed that activation of the nuclear factor kappaB (NF-kappaB), a hallmark of inflammatory responses that is frequently detected in tumours, may constitute a missing link between inflammation and cancer. To test this hypothesis, we studied the Mdr2-knockout mouse strain, which spontaneously develops cholestatic hepatitis followed by hepatocellular carcinoma, a prototype of inflammation-associated cancer. We monitored hepatitis and cancer progression in Mdr2-knockout mice, and here we show that the inflammatory process triggers hepatocyte NF-kappaB through upregulation of tumour-necrosis factor-alpha (TNFalpha) in adjacent endothelial and inflammatory cells. Switching off NF-kappaB in mice from birth to seven months of age, using a hepatocyte-specific inducible IkappaB-super-repressor transgene, had no effect on the course of hepatitis, nor did it affect early phases of hepatocyte transformation. By contrast, suppressing NF-kappaB inhibition through anti-TNFalpha treatment or induction of IkappaB-super-repressor in later stages of tumour development resulted in apoptosis of transformed hepatocytes and failure to progress to hepatocellular carcinoma. Our studies thus indicate that NF-kappaB is essential for promoting inflammation-associated cancer, and is therefore a potential target for cancer prevention in chronic inflammatory diseases.},
author = {Pikarsky, Eli and Porat, Rinnat M and Stein, Ilan and Abramovitch, Rinat and Amit, Sharon and Kasem, Shafika and Gutkovich-Pyest, Elena and Urieli-Shoval, Simcha and Galun, Eithan and Ben-Neriah, Yinon},
doi = {10.1038/nature02924},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Pikarsky et al. - 2004 - NF-kappaB functions as a tumour promoter in inflammation-associated cancer.pdf:pdf},
isbn = {1476-4687 (Electronic)$\backslash$r0028-0836 (Linking)},
issn = {0028-0836},
journal = {Nature},
keywords = {cancer,inflammation},
mendeley-tags = {cancer,inflammation},
pages = {461--466},
pmid = {15329734},
title = {{NF-kappaB functions as a tumour promoter in inflammation-associated cancer.}},
volume = {431},
year = {2004}
}
@incollection{Smyth2005,
abstract = {Abstract A survey is given of differential expression analyses using the linear modeling features of the limma package. The chapter starts with the simplest replicated designs and progresses through experiments with two or more groups, direct designs, factorial designs ...},
archivePrefix = {arXiv},
arxivId = {16495579},
author = {Smyth, G K},
booktitle = {Bioinforma. Comput. Biol. Solut. Using R Bioconductor},
doi = {10.1007/0-387-29362-0_23},
eprint = {16495579},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Smyth - 2005 - Limma linear models for microarray data.pdf:pdf},
isbn = {1431-8776},
issn = {1544-6115},
pages = {397--420},
pmid = {16495579},
title = {{Limma: linear models for microarray data}},
year = {2005}
}
@article{Nik-Zainal2012,
abstract = {All cancers carry somatic mutations. The patterns of mutation in cancer genomes reflect the DNA damage and repair processes to which cancer cells and their precursors have been exposed. To explore these mechanisms further, we generated catalogs of somatic mutation from 21 breast cancers and applied mathematical methods to extract mutational signatures of the underlying processes. Multiple distinct single- and double-nucleotide substitution signatures were discernible. Cancers with BRCA1 or BRCA2 mutations exhibited a characteristic combination of substitution mutation signatures and a distinctive profile of deletions. Complex relationships between somatic mutation prevalence and transcription were detected. A remarkable phenomenon of localized hypermutation, termed "kataegis," was observed. Regions of kataegis differed between cancers but usually colocalized with somatic rearrangements. Base substitutions in these regions were almost exclusively of cytosine at TpC dinucleotides. The mechanisms underlying most of these mutational signatures are unknown. However, a role for the APOBEC family of cytidine deaminases is proposed. {\textcopyright} 2012 Elsevier Inc.},
author = {Nik-Zainal, Serena and Alexandrov, Ludmil B. and Wedge, David C. and {Van Loo}, Peter and Greenman, Christopher D. and Raine, Keiran and Jones, David and Hinton, Jonathan and Marshall, John and Stebbings, Lucy A. and Menzies, Andrew and Martin, Sancha and Leung, Kenric and Chen, Lina and Leroy, Catherine and Ramakrishna, Manasa and Rance, Richard and Lau, King Wai and Mudie, Laura J. and Varela, Ignacio and McBride, David J. and Bignell, Graham R. and Cooke, Susanna L. and Shlien, Adam and Gamble, John and Whitmore, Ian and Maddison, Mark and Tarpey, Patrick S. and Davies, Helen R. and Papaemmanuil, Elli and Stephens, Philip J. and McLaren, Stuart and Butler, Adam P. and Teague, Jon W. and J{\"{o}}nsson, G{\"{o}}ran and Garber, Judy E. and Silver, Daniel and Miron, Penelope and Fatima, Aquila and Boyault, Sandrine and Langerod, Anita and Tutt, Andrew and Martens, John W M and Aparicio, Samuel A J R and Borg, {\AA}ke and Salomon, Anne Vincent and Thomas, Gilles and Borresen-Dale, Anne Lise and Richardson, Andrea L. and Neuberger, Michael S. and Futreal, P. Andrew and Campbell, Peter J. and Stratton, Michael R.},
doi = {10.1016/j.cell.2012.04.024},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Nik-Zainal et al.{\_}2012{\_}Mutational processes molding the genomes of 21 breast cancers.pdf:pdf},
isbn = {1097-4172 (Electronic)$\backslash$r0092-8674 (Linking)},
issn = {00928674},
journal = {Cell},
keywords = {kataegis},
mendeley-tags = {kataegis},
pages = {979--993},
pmid = {22608084},
title = {{Mutational processes molding the genomes of 21 breast cancers}},
volume = {149},
year = {2012}
}
@article{Satyamoorthy2003,
author = {Satyamoorthy, Kapaettu and Li, Gang and Gerrero, Michelle R and Brose, Marcia S and Volpe, Patricia and Weber, Barbara L and Belle, Patricia Van and Elder, David E and Herlyn, Meenhard},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Satyamoorthy et al. - 2003 - Constitutive Mitogen-activated Protein Kinase Activation in Melanoma Is Mediated by Both BRAF Mutations and.pdf:pdf},
journal = {Cancer Res.},
keywords = {cancer},
mendeley-tags = {cancer},
pages = {756--759},
title = {{Constitutive Mitogen-activated Protein Kinase Activation in Melanoma Is Mediated by Both BRAF Mutations and Autocrine Growth Factor Stimulation Advances in Brief Constitutive Mitogen-activated Protein Kinase Activation in Melanoma Is Mediated by Both BRAF}},
volume = {63},
year = {2003}
}
@article{Ioannidis2009,
author = {Ioannidis, John P A and Allison, David B and Ball, Catherine A and Coulibaly, Issa and Cui, Xiangqin and Culhane, Aed{\'{i}}n C and Falchi, Mario and Furlanello, Cesare and Game, Laurence and Jurman, Giuseppe and Mangion, Jon and Mehta, Tapan and Nitzberg, Michael and Page, Grier P and Petretto, Enrico and Noort, Vera Van},
doi = {10.1038/ng.295},
file = {:Users/rikutakei/Downloads/papers/ng.295.pdf:pdf},
journal = {Nat. Genet.},
number = {2},
pages = {149--155},
title = {{a n a ly s i s Repeatability of published microarray gene expression analyses}},
volume = {41},
year = {2009}
}
@article{Armstrong2001,
abstract = {There is persuasive evidence that each of the three main types of skin cancer, basal cell carcinoma (PCC), squamous cell carcinoma (SCC) and melanoma, is caused by sun exposure. The incidence rate of each is higher in fairer skinned, sun-sensitive rather than darker skinned, less sun-sensitive people; risk increases with increasing ambient solar radiation; the highest densities are on the most sun exposed parts of the body and the lowest on the least exposed; and they are associated in individuals with total (mainly SCC), occupational (mainly SCC) and non-occupational or recreational sun exposure (mainly melanoma and BCC) and a history of sunburn and presence of benign sun damage in the skin. That UV radiation specifically causes these skin cancers depends on indirect inferences from the action spectrum of solar radiation for skin cancer from studies in animals and the action spectrum for dipyrimidine dimers and evidence that presumed causative mutations for skin cancer arise most commonly at dipyrimidine sites. Sun protection is essential if skin cancer incidence is to be reduced. The epidemiological data suggest that in implementing sun protection an increase in intermittency of exposure should be avoided, that sun protection will have the greatest impact if achieved as early as possible in life and that it will probably have an impact later in life, especially in those who had high childhood exposure to solar radiation. ?? 2001 Elsevier Science B.V. All rights reserved.},
author = {Armstrong, Bruce K. and Kricker, Anne},
doi = {10.1016/S1011-1344(01)00198-1},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Armstrong, Kricker - 2001 - The epidemiology of UV induced skin cancer.pdf:pdf},
isbn = {6199334183},
issn = {10111344},
journal = {J. Photochem. Photobiol. B Biol.},
keywords = {Basal cell carcinoma,Cutaneous malignant melanoma,Squamous cell carcinoma,UVA,UVB,cancer,environmental factors,uv},
mendeley-tags = {cancer,environmental factors,uv},
number = {1-3},
pages = {8--18},
pmid = {11684447},
title = {{The epidemiology of UV induced skin cancer}},
volume = {63},
year = {2001}
}
@article{Adrian1985,
abstract = {A radioimmunoassay has been developed for the new intestinal hormonal peptide tyrosine tyrosine [peptide YY (PYY)]. Peptide YY concentrations were measured in separated layers of the human gastrointestinal tract, where PYY was found exclusively in the mucosal epithelium which contained the endocrine cells. Peptide YY was found throughout the small intestine, in very low concentrations (5 pmol/g) in duodenum (6 pmol/g) and jejunum (5 pmol/g), but in higher concentrations in the terminal ileum (84 pmol/g). High concentrations were found throughout the colon (ascending 82 pmol/g, sigmoid 196 pmol/g), being maximum in the rectum (480 pmol/g). The major molecular form of PYY-like immunoreactivity in human intestine appeared to be identical to pure porcine hormone, both as judged by gel permeation chromatography and by reverse-phase high-pressure liquid chromatography. Basal plasma concentrations of PYY were low but rose in response to food, remaining elevated for several hours postprandially. The known potent biologic actions of PYY, its high concentrations in gut endocrine cells, and its release into the circulation after a normal meal suggest that this peptide may function physiologically as a circulating gut hormone.},
author = {Adrian, T E and Ferri, G L and Bacarese-Hamilton, A J and Fuessl, H S and Polak, J M and Bloom, S R},
doi = {S0016508585003110 [pii]},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Adrian et al. - 1985 - Human distribution and release of a putative new gut hormone, peptide YY.pdf:pdf},
isbn = {0016-5085 (Print)$\backslash$r0016-5085 (Linking)},
issn = {0016-5085},
journal = {Gastroenterology},
keywords = {Adult,Aged,Chromatography,Eating,Energy Intake,Gastrointestinal Hormones,Gastrointestinal Hormones: metabolism,Gel,High Pressure Liquid,Histocytochemistry,Humans,Immunochemistry,Intestines,Intestines: cytology,Intestines: metabolism,Intestines: ultrastructure,Middle Aged,Pancreatic Polypeptide,Pancreatic Polypeptide: metabolism,Peptide YY,Peptides,Peptides: metabolism,Radioimmunoassay,obesity},
mendeley-tags = {obesity},
number = {5},
pages = {1070--1077},
pmid = {3840109},
title = {{Human distribution and release of a putative new gut hormone, peptide YY.}},
volume = {89},
year = {1985}
}
@article{Castle1910,
author = {Castle, W. E. and Little, C. C.},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Castle, Little - 1910 - On a modified mendelian ratio among yellow mice.pdf:pdf},
journal = {Science (80-. ).},
keywords = {agouti},
mendeley-tags = {agouti},
number = {833},
pages = {868--870},
title = {{On a modified mendelian ratio among yellow mice}},
volume = {32},
year = {1910}
}
@book{Garrow1988,
address = {London},
author = {Garrow, J. S.},
keywords = {obesity},
mendeley-tags = {obesity},
pages = {1--16},
publisher = {Churchill Livingstone},
title = {{Obesity and related diseases}},
year = {1988}
}
@article{Teng2008,
abstract = {This brief review discusses the role of the immune system in tumor development, covering a history of cancer immunity and a summary of the concept of cancer immunoediting, including its three phases: elimination, equilibrium, and escape. The latter half of this review then focuses specifically on the equilibrium phase, making note of previous work, suggesting that immunity might maintain cancer in a dormant state, and concluding with a description of a tractable mouse model unequivocally demonstrating that immunity can indeed hold preformed cancer in check. These findings form a framework for future studies aimed at validating immune-mediated cancer dormancy in humans with the hopes of devising new, immunotherapeutic strategies to treat established cancer.},
author = {Teng, M W and Swann, J B and Koebel, C M and Schreiber, R D and Smyth, M J},
doi = {10.1189/jlb.1107774},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Teng et al. - 2008 - Immune-mediated dormancy an equilibrium with cancer.pdf:pdf},
isbn = {0741-5400 (Print)$\backslash$r0741-5400 (Linking)},
issn = {0741-5400},
journal = {J. Leukoc. Biol.},
keywords = {*Immune System,Animal,Animals,Disease Models,Humans,Interferon-gamma/immunology,Interleukin-12/immunology,Mice,Neoplasms/*immunology/*pathology,Neovascularization,Pathologic/immunology,T-Lymphocytes/immunology,Tumor Escape/*immunology,cancer,immune},
mendeley-tags = {cancer,immune},
number = {4},
pages = {988--993},
pmid = {18515327},
title = {{Immune-mediated dormancy: an equilibrium with cancer}},
volume = {84},
year = {2008}
}
@article{DeBerardinis2008,
abstract = {Cell proliferation requires nutrients, energy, and biosynthetic activity to duplicate all macromolecular components during each passage through the cell cycle. It is therefore not surprising that metabolic activities in proliferating cells are fundamentally different from those in nonproliferating cells. This review examines the idea that several core fluxes, including aerobic glycolysis, de novo lipid biosynthesis, and glutamine-dependent anaplerosis, form a stereotyped platform supporting proliferation of diverse cell types. We also consider regulation of these fluxes by cellular mediators of signal transduction and gene expression, including the phosphatidylinositol 3-kinase (PI3K)/Akt/mTOR system, hypoxia-inducible factor 1 (HIF-1), and Myc, during physiologic cell proliferation and tumorigenesis. ?? 2008 Elsevier Inc. All rights reserved.},
author = {DeBerardinis, Ralph J. and Lum, Julian J. and Hatzivassiliou, Georgia and Thompson, Craig B.},
doi = {10.1016/j.cmet.2007.10.002},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/DeBerardinis et al. - 2008 - The Biology of Cancer Metabolic Reprogramming Fuels Cell Growth and Proliferation.pdf:pdf},
isbn = {1550-4131 (Print) 1550-4131 (Linking)},
issn = {15504131},
journal = {Cell Metab.},
keywords = {cancer,energy},
mendeley-tags = {cancer,energy},
number = {1},
pages = {11--20},
pmid = {18177721},
title = {{The Biology of Cancer: Metabolic Reprogramming Fuels Cell Growth and Proliferation}},
volume = {7},
year = {2008}
}
@misc{reactome,
author = {Lightenberg, Willem},
title = {{reactome.db: A set of annotation maps for reactome}},
year = {2016}
}
@article{Bhowmick2004,
abstract = {3. Measures for access, participation, and progression – Academies must encourage, support, and celebrate the contributions of women to scientific discovery and application. – This chapter considers programmes to increase the numbers of women progressing through science and engineering education, training, and careers. These are needed while women are still a minority. Briefly, these activities cover enhancement of visibility, the importance of role models, access to mentoring and networks and initiatives that provide earmarked resources to women in launching their careers or reestablishing them after a family-related break. In parallel, good management practice must be implemented to make organizations inclusive. Academies, individually and jointly, are requested to support ongoing programmes, and to develop measures of their own that give recognition to women scientists.},
author = {Bhowmick, Neil a and Neilson, Eric G and Moses, Harold L},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Bhowmick, Neilson, Moses - 2004 - Stromal fibroblasts in cancer initiation and progression.pdf:pdf},
journal = {Nature},
keywords = {cancer},
mendeley-tags = {cancer},
number = {November},
pages = {332--337},
title = {{Stromal fibroblasts in cancer initiation and progression}},
volume = {432},
year = {2004}
}
@article{Huang2009,
abstract = {Functional analysis of large gene lists, derived in most cases from emerging high-throughput genomic, proteomic and bioinformatics scanning approaches, is still a challenging and daunting task. The gene-annotation enrichment analysis is a promising high-throughput strategy that increases the likelihood for investigators to identify biological processes most pertinent to their study. Approximately 68 bioinformatics enrichment tools that are currently available in the community are collected in this survey. Tools are uniquely categorized into three major classes, according to their underlying enrichment algorithms. The comprehensive collections, unique tool classifications and associated questions/issues will provide a more comprehensive and up-to-date view regarding the advantages, pitfalls and recent trends in a simpler tool-class level rather than by a tool-by-tool approach. Thus, the survey will help tool designers/developers and experienced end users understand the underlying algorithms and pertinent details of particular tool categories/tools, enabling them to make the best choices for their particular research interests.},
author = {Huang, Da Wei and Sherman, Brad T. and Lempicki, Richard A.},
doi = {10.1093/nar/gkn923},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Huang, Sherman, Lempicki - 2009 - Bioinformatics enrichment tools Paths toward the comprehensive functional analysis of large gene lists.pdf:pdf},
isbn = {1362-4962 (Electronic)$\backslash$r0305-1048 (Linking)},
issn = {03051048},
journal = {Nucleic Acids Res.},
number = {1},
pages = {1--13},
pmid = {19033363},
title = {{Bioinformatics enrichment tools: Paths toward the comprehensive functional analysis of large gene lists}},
volume = {37},
year = {2009}
}
@article{Chan2010,
abstract = {Obesity is a public health problem that has become epidemic worldwide. Substantial literature has emerged to show that overweight and obesity are major causes of co-morbidities, including type II diabetes, cardiovascular diseases, various cancers and other health problems, which can lead to further morbidity and mortality. The related health care costs are also substantial. Therefore, a public health approach to develop population-based strategies for the prevention of excess weight gain is of great importance. However, public health intervention programs have had limited success in tackling the rising prevalence of obesity. This paper reviews the definition of overweight and obesity and the variations with age and ethnicity; health consequences and factors contributing to the development of obesity; and critically reviews the effectiveness of current public health strategies for risk factor reduction and obesity prevention.},
author = {Chan, Ruth S M and Woo, Jean},
doi = {10.3390/ijerph7030765},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Chan, Woo - 2010 - Prevention of overweight and obesity How effective is the current public health approach.pdf:pdf},
isbn = {1660-4601 (Electronic)$\backslash$r1660-4601 (Linking)},
issn = {16604601},
journal = {Int. J. Environ. Res. Public Health},
keywords = {Obesity,Prevention,Public health,obesity},
mendeley-tags = {obesity},
number = {3},
pages = {765--783},
pmid = {20617002},
title = {{Prevention of overweight and obesity: How effective is the current public health approach}},
volume = {7},
year = {2010}
}
@article{SuHuang1997,
abstract = {Deregulation of signaling by the epidermal growth factor receptor (EGFR) is common in human malignancy progression. One mutant EGFR (variously named DeltaEGFR, de2-7 EGFR, or EGFRvIII), which occurs frequently in human cancers, lacks a portion of the extracellular ligand-binding domain due to genomic deletions that eliminate exons 2 to 7 and confers a dramatic enhancement of brain tumor cell tumorigenicity in vivo. In order to dissect the molecular mechanisms of this activity, we analyzed location, autophosphorylation, and attenuation of the mutant receptors. The mutant receptors were expressed on the cell surface and constitutively autophosphorylated at a significantly decreased level compared with wild-type EGFR activated by ligand treatment. Unlike wild-type EGFR, the constitutively active DeltaEGFR were not down-regulated, suggesting that the altered conformation of the mutant did not result in exposure of receptor sequence motifs required for endocytosis and lysosomal sorting. Mutational analysis showed that the enhanced tumorigenicity was dependent on intrinsic tyrosine kinase activity and was mediated through the carboxyl terminus. In contrast with wild-type receptor, mutation of any major tyrosine autophosphorylation site abolished these activities suggesting that the biological functions of DeltaEGFR are due to low constitutive activation with mitogenic effects amplified by failure to attenuate signaling by receptor down-regulation.},
author = {{Su Huang}, H. J. and Nagane, Motoo and Klingbeil, Candice K. and Lin, Hong and Nishikawa, Ryo and Ji, Xiang Dong and Huang, Chun Ming and Gill, Gordon N. and Wiley, H. Steven and Cavenee, Webster K.},
doi = {10.1074/jbc.272.5.2927},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Su Huang et al. - 1997 - The enhanced tumorigenic activity of a mutant epidermal growth factor receptor common in human cancers is media.pdf:pdf},
isbn = {0021-9258 (Print)},
issn = {00219258},
journal = {J. Biol. Chem.},
keywords = {cancer},
mendeley-tags = {cancer},
number = {5},
pages = {2927--2935},
pmid = {9006938},
title = {{The enhanced tumorigenic activity of a mutant epidermal growth factor receptor common in human cancers is mediated by threshold levels of constitutive tyrosine phosphorylation and unattenuated signaling}},
volume = {272},
year = {1997}
}
@article{Mckeown1994,
author = {McKeown-Eyssen, Gail},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/McKeown-Eyssen - 1994 - Epidemiology Triglycerides of Colorectal and or Plasma Cancer Glucose Revisited Associated Are Serum with Risk.pdf:pdf},
journal = {Cancer Epidemiol. Biomarkers Prev.},
keywords = {insulin cancer hypothesis},
mendeley-tags = {insulin cancer hypothesis},
number = {December},
pages = {687-- 695},
title = {{Epidemiology Triglycerides of Colorectal and / or Plasma Cancer Glucose Revisited : Associated Are Serum with Risk ?}},
volume = {3},
year = {1994}
}
@article{Giovannucci1995,
author = {Giovannucci, Edward},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Giovannucci - 1995 - Insulin and colon cancer.pdf:pdf},
journal = {Cancer Causes Control},
keywords = {colon cancer,diet,hyperinsulinemia,insulin,insulin cancer hypothesis,obesity,physical inactivity},
mendeley-tags = {insulin cancer hypothesis},
number = {18},
pages = {164--179},
title = {{Insulin and colon cancer}},
volume = {6},
year = {1995}
}
@article{Jenabi2011,
abstract = {Conflict and different studies was done about the effect of body mass index on delivery outcomes. Our objective was to effect body mass index on delivery outcomes in hospital of Tamin Ejtemaee in city of Hamedan. Women admitted in unit of labor were invited to participate in this study. During a 3-mounth period, 1272 eligible women gave consent and were randomized in this study. Chi square test and wilcoxon were used for data's analyze. Obesity and overweight of pregnancy was significant correlation with the before parity, increase of weight neonate, gestational age, duration of active phase and second stage of labor. Overweight and obesity pregnancy is associated with adverse pregnancy outcome in women. ?? 2011 Published by Elsevier Ltd.},
author = {Jenabi, Ensiyeh and AslToghiri, Maryam},
doi = {10.1016/j.sbspro.2011.11.089},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Jenabi, AslToghiri - 2011 - The effect of body mass index on delivery outcomes.pdf:pdf},
issn = {18770428},
journal = {Procedia - Soc. Behav. Sci.},
keywords = {Body Mass Index,Caesarean section,Delivery outcomes,Gestational age,Neonate weight},
pages = {465--469},
publisher = {Elsevier Ltd},
title = {{The effect of body mass index on delivery outcomes}},
volume = {28},
year = {2011}
}
@article{Cowley2001,
abstract = {The administration of leptin to leptin-deficient humans, and the analogous Lepob/Lepob mice, effectively reduces hyperphagia and obesity. But common obesity is associated with elevated leptin, which suggests that obese humans are resistant to this adipocyte hormone. In addition to regulating long-term energy balance, leptin also rapidly affects neuronal activity. Proopiomelanocortin (POMC) and neuropeptide-Y types of neurons in the arcuate nucleus of the hypothalamus are both principal sites of leptin receptor expression and the source of potent neuropeptide modulators, melanocortins and neuropeptide Y, which exert opposing effects on feeding and metabolism. These neurons are therefore ideal for characterizing leptin action and the mechanism of leptin resistance; however, their diffuse distribution makes them difficult to study. Here we report electrophysiological recordings on POMC neurons, which we identified by targeted expression of green fluorescent protein in transgenic mice. Leptin increases the frequency of action potentials in the anorexigenic POMC neurons by two mechanisms: depolarization through a nonspecific cation channel; and reduced inhibition by local orexigenic neuropeptide-Y/GABA (gamma-aminobutyric acid) neurons. Furthermore, we show that melanocortin peptides have an autoinhibitory effect on this circuit. On the basis of our results, we propose an integrated model of leptin action and neuronal architecture in the arcuate nucleus of the hypothalamus.},
author = {Cowley, M a and Smart, J L and Rubinstein, M and Cerd{\'{a}}n, M G and Diano, S and Horvath, T L and Cone, R D and Low, M J},
doi = {10.1038/35078085},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Cowley et al. - 2001 - Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus.pdf:pdf},
isbn = {0028-0836 (Print) 0028-0836 (Linking)},
issn = {0028-0836},
journal = {Nature},
keywords = {leptin},
mendeley-tags = {leptin},
number = {6836},
pages = {480--484},
pmid = {11373681},
title = {{Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus.}},
volume = {411},
year = {2001}
}
@article{Vassilev2004,
abstract = {MDM2 binds the p53 tumor suppressor protein with high affinity and negatively modulates its transcriptional activity and stability. Overexpression of MDM2, found in many human tumors, effectively impairs p53 function. Inhibition of MDM2-p53 interaction can stabilize p53 and may offer a novel strategy for cancer therapy. Here, we identify potent and selective small-molecule antagonists of MDM2 and confirm their mode of action through the crystal structures of complexes. These compounds bind MDM2 in the p53-binding pocket and activate the p53 pathway in cancer cells, leading to cell cycle arrest, apoptosis, and growth inhibition of human tumor xenografts in nude mice. [ABSTRACT FROM AUTHOR]},
archivePrefix = {arXiv},
arxivId = {NIHMS150003},
author = {Vassilev, Lyubomir T and Vu, Binh T and Craves, Bradford and Carvajal, Daisy and Podlaski, Frank and Filipovic, Zoran and Kong, Norman and Kammlott, Ursula and Lukacs, Christine and Klein, Christian and Fotouhi, Nader and Liu, Emily A},
doi = {10.1126/science.1092472},
eprint = {NIHMS150003},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Vassilev et al. - 2004 - In Vivo Activation of the p53 Pathway by Small-MoleculeAntagonists of MDM2.pdf:pdf},
isbn = {1095-9203 (Electronic)$\backslash$r0036-8075 (Linking)},
issn = {00368075},
journal = {Science (80-. ).},
keywords = {APOPTOSIS,CANCER treatment,CELL cycle,DNA-binding proteins,P53 protein,TUMORS,XENOGRAFTS,mdm2,p53},
mendeley-tags = {mdm2,p53},
number = {5659},
pages = {844--848},
pmid = {14704432},
title = {{In Vivo Activation of the p53 Pathway by Small-MoleculeAntagonists of MDM2.}},
volume = {303},
year = {2004}
}
@article{Edgar2002,
abstract = {The Gene Expression Omnibus (GEO) project was initiated in response to the growing demand for a public repository for high-throughput gene expression data. GEO provides a flexible and open design that facilitates submission, storage and retrieval of heterogeneous data sets from high-throughput gene expression and genomic hybridization experiments. GEO is not intended to replace in house gene expression databases that benefit from coherent data sets, and which are constructed to facilitate a particular analytic method, but rather complement these by acting as a tertiary, central data distribution hub. The three central data entities of GEO are platforms, samples and series, and were designed with gene expression and genomic hybridization experiments in mind. A platform is, essentially, a list of probes that define what set of molecules may be detected. A sample describes the set of molecules that are being probed and references a single platform used to generate its molecular abundance data. A series organizes samples into the meaningful data sets which make up an experiment. The GEO repository is publicly accessible through the World Wide Web at http://www.ncbi.nlm.nih.gov/geo.},
author = {Edgar, Ron and Domrachev, Michael and Lash, Alex E},
doi = {10.1093/nar/30.1.207},
file = {:Users/rikutakei/Documents/Mendeley Desktop/Edgar, Domrachev, Lash{\_}2002{\_}Gene Expression Omnibus NCBI gene expression and hybridization array data repository.pdf:pdf},
isbn = {1362-4962 (Electronic)$\backslash$r0305-1048 (Linking)},
issn = {1362-4962},
journal = {Nucleic Acids Res.},
number = {1},
pages = {207--210},
pmid = {11752295},
title = {{Gene Expression Omnibus: NCBI gene expression and hybridization array data repository.}},
volume = {30},
year = {2002}
}
@article{Ashford2015,
author = {Ashford, Nicholas A and Bauman, Patricia and Brown, Halina S and Clapp, Richard W and Finkel, Adam M and Gee, David and Dale, B and Martuzzi, Marco and Sasco, Annie J and Marsh, George Perkins},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Ashford et al. - 2015 - Cancer risk Role of environment Cancer risk Tumors excluded Cancer risk Role of chance overstated Cancer risk.pdf:pdf},
keywords = {cancer,environmental factors},
mendeley-tags = {cancer,environmental factors},
number = {160},
title = {{Cancer risk : Role of environment Cancer risk : Tumors excluded Cancer risk : Role of chance overstated Cancer risk : Prevention is crucial Cancer risk : Many factors contribute}},
volume = {347},
year = {2015}
}
@article{Basen2011,
abstract = {The prevalence of overweight and obesity is increasing worldwide, and the evidence base for a link between obesity and cancer is growing. In the United States, approximately 85,000 new cancer cases per year are related to obesity. Recent research has found that as the body mass index increases by 5 kg/m2, cancer mortality increases by 10{\%}. Additionally, studies of patients who have had bariatric surgery for weight loss report reductions in cancer incidence and mortality, particularly for women. The goal of this review is to provide an update of recent research, with a focus on epidemiologic studies on the link between obesity and cancer. In addition, we will briefly review hypothesized mechanisms underlying the relationship between obesity and cancer. High priorities for future research involve additional work on the underlying mechanisms, and trials to examine the effect of lifestyle behavior change and weight loss interventions on cancer and intermediate biomarkers.},
author = {Basen-Engquist, Karen and Chang, Maria},
doi = {10.1007/s11912-010-0139-7},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Basen-Engquist, Chang - 2011 - Obesity and cancer risk Recent review and evidence.pdf:pdf},
isbn = {1534-6269 (Electronic)$\backslash$r1523-3790 (Linking)},
issn = {15233790},
journal = {Curr. Oncol. Rep.},
keywords = {Adipokines,Cancer risk,Hypoxia,Insulin,Insulin-like growth factors,Intervention,Neoplasm,Obesity,Overweight,Oxidative stress,Review,Sex steroid hormones,obesity and cancer},
mendeley-tags = {obesity and cancer},
number = {1},
pages = {71--76},
pmid = {21080117},
title = {{Obesity and cancer risk: Recent review and evidence}},
volume = {13},
year = {2011}
}
@article{Niswender2004,
abstract = {Despite an alarming increase in the burden of obesity worldwide, body adiposity seems to be a regulated physiological variable. Regulation of adiposity occurs through a classical endocrine feedback loop, in which the pancreatic ??-cell-derived hormone insulin and the adipocyte-derived hormone leptin signal the status of body energy stores to the hypothalamus. Recent advances in our understanding of the signal transduction mechanisms used by insulin and leptin in the hypothalamus to modulate neuronal firing suggest that intracellular cross-talk occurs at several levels and is a potentially important determinant of regulated body weight. These pathways are thus an attractive target for pharmacological intervention in the treatment of obesity.},
author = {Niswender, Kevin D. and Baskin, Denis G. and Schwartz, Michael W.},
doi = {10.1016/j.tem.2004.07.009},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Niswender, Baskin, Schwartz - 2004 - Insulin and its evolving partnership with leptin in the hypothalamic control of energy homeostasis.pdf:pdf},
isbn = {1043-2760},
issn = {10432760},
journal = {Trends Endocrinol. Metab.},
keywords = {insulin,leptin},
mendeley-tags = {insulin,leptin},
number = {8},
pages = {362--369},
pmid = {15380807},
title = {{Insulin and its evolving partnership with leptin in the hypothalamic control of energy homeostasis}},
volume = {15},
year = {2004}
}
@article{Gilbert2013,
abstract = {Obesity is a problem of epidemic proportions in many developed nations. Increased body mass index and obesity are associated with a significantly worse outcome for many cancers. Breast cancer risk in the postmenopausal setting and poor disease outcome for all patients is significantly augmented in overweight and obese individuals. The expansion of fat tissue involves a complex interaction of endocrine factors known as adipokines and cytokines. High cytokine levels in primary breast cancers and in the circulation of affected patients have been associated with poor outcome. This review summarizes the how cytokine production in obese adipose tissue creates a chronic inflammatory microenvironment that favors tumor cell motility, invasion, and epithelial-mesenchymal transition to enhance the metastatic potential of tumor cells. Many of the cytokines associated with a proinflammatory state are not only upregulated in obese adipose tissue but may also stimulate the self-renewal of cancer stem cells. Thus, enhanced cytokine production in obese adipose tissue may serve both as a chemoattractant for invading cancers and to augment their malignant potential. These new mechanistic insights suggest that the current obesity epidemic will presage a significant increase in cancer incidence, morbidity, and mortality in the next few decades.},
author = {Gilbert, Candace a and Slingerland, Joyce M},
doi = {10.1146/annurev-med-121211-091527},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Gilbert, Slingerland - 2013 - Cytokines, obesity, and cancer new insights on mechanisms linking obesity to cancer risk and progression.pdf:pdf},
isbn = {0066-4219},
issn = {1545-326X},
journal = {Annu. Rev. Med.},
keywords = {Body Mass Index,Cytokines,Cytokines: metabolism,Disease Progression,Humans,Incidence,Neoplasms,Neoplasms: complications,Neoplasms: epidemiology,Neoplasms: metabolism,Obesity,Obesity: complications,Obesity: epidemiology,Obesity: metabolism,Risk Factors,World Health},
number = {October},
pages = {45--57},
pmid = {23121183},
title = {{Cytokines, obesity, and cancer: new insights on mechanisms linking obesity to cancer risk and progression.}},
volume = {64},
year = {2013}
}
@misc{kegg,
author = {Carlson, M},
title = {{KEGG.db: A set of annotation maps for KEGG}},
year = {2016}
}
@article{Kim2007,
abstract = {Cancer immune surveillance is considered to be an important host protection process to inhibit carcinogenesis and to maintain cellular homeostasis. In the interaction of host and tumour cells, three essential phases have been proposed: elimination, equilibrium and escape, which are designated the 'three E's'. Several immune effector cells and secreted cytokines play a critical role in pursuing each process. Nascent transformed cells can initially be eliminated by an innate immune response such as by natural killer cells. During tumour progression, even though an adaptive immune response can be provoked by antigen-specific T cells, immune selection produces tumour cell variants that lose major histocompatibility complex class I and II antigens and decreases amounts of tumour antigens in the equilibrium phase. Furthermore, tumour-derived soluble factors facilitate the escape from immune attack, allowing progression and metastasis. In this review, the central roles of effector cells and cytokines in tumour immunity, and the escape mechanisms of tumour cells during tumour progression are discussed.},
author = {Kim, Ryungsa and Emi, Manabu and Tanabe, Kazuaki},
doi = {10.1111/j.1365-2567.2007.02587.x},
file = {:Users/rikutakei/Library/Application Support/Mendeley Desktop/Downloaded/Kim, Emi, Tanabe - 2007 - Cancer immunoediting from immune surveillance to immune escape.pdf:pdf},
isbn = {9780123725516},
issn = {0019-2805},
journal = {Immunology},
keywords = {02587,10,1111,1365-2567,2007,accepted 23 january 2007,cancer,doi,immune,immune escape,immune surveillance,immunoediting,j,january 2007,received 2 november 2006,revised 5,x},
mendeley-tags = {cancer,immune},
number = {1},
pages = {1--14},
pmid = {17386080},
title = {{Cancer immunoediting from immune surveillance to immune escape.}},
volume = {121},
year = {2007}
}