text:
.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 = {:home/riku/Documents/Mendeley Desktop/Yusuf et al/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}
}
@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{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 = {:home/riku/Documents/Mendeley Desktop/World Health Organisation/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},
pages = {60},
pmid = {20963782},
primaryClass = {arXiv:gr-qc},
title = {{Global recommendations on physical activity for health}},
year = {2010}
}
@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 = {:home/riku/Documents/Mendeley Desktop/McLaren/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{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 = {:home/riku/Documents/Mendeley Desktop/Frayling et al/Frayling et al.{\_}2007{\_}A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity.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{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 = {:home/riku/Documents/Mendeley Desktop/Osborne, Schiff/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{Hanahan2000,
author = {Hanahan, Douglas and Weinberg, Robert A.},
doi = {10.1016/S0092-8674(00)81683-9},
file = {:home/riku/Documents/Mendeley Desktop/Hanahan, Weinberg/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{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 = {:home/riku/Documents/Mendeley Desktop/Neel/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{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 = {:home/riku/Documents/Mendeley Desktop/Kublaoui et al/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{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 = {:home/riku/Documents/Mendeley Desktop/Challis et al/Challis et al.{\_}2002{\_}A missense mutation disrupting a dibasic prohormone processing site in pro-opiomelanocortin (POMC) increases suscept.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}
}
@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{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 = {:home/riku/Documents/Mendeley Desktop/Dubern et al/Dubern et al.{\_}2001{\_}Mutational analysis of melanocortin-4 receptor, agouti-related protein, and alpha-melanocyte-stimulating hormone gene.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{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 = {:home/riku/Documents/Mendeley Desktop/Freedman et al/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{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 = {:home/riku/Documents/Mendeley Desktop/Farooqi et al/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}
}
@article{Waalen2014,
abstract = {The heritability of obesity has long been appreciated and the genetics of obesity has been the focus of intensive study for decades. Early studies elucidating genetic factors involved in rare monogenic and syndromic forms of extreme obesity focused attention on dysfunction of hypothalamic leptin-related pathways in the control of food intake as a major contributor. Subsequent genome-wide association studies of common genetic variants identified novel loci that are involved in more common forms of obesity across populations of diverse ethnicities and ages. The subsequent search for factors contributing to the heritability of obesity not explained by these 2 approaches ("missing heritability") has revealed additional rare variants, copy number variants, and epigenetic changes that contribute. Although clinical applications of these findings have been limited to date, the increasing understanding of the interplay of these genetic factors with environmental conditions, such as the increased availability of high calorie foods and decreased energy expenditure of sedentary lifestyles, promises to accelerate the translation of genetic findings into more successful preventive and therapeutic interventions.},
author = {Waalen, Jill},
doi = {10.1016/j.trsl.2014.05.010},
file = {:home/riku/Documents/Mendeley Desktop/Waalen/Waalen{\_}2014{\_}The genetics of human obesity.pdf:pdf},
isbn = {1931-5244},
issn = {18781810},
journal = {Transl. Res.},
keywords = {BMI = Body mass index,CNV = Copy number variants,CPG = cytosine-phosphate-guanine,GCTA = Genome-wide complex trait analysis,GWAS = Genome-wide association study,ITMAT = Institute for Translational Medicine and T,MAF = Minor allele frequency,PPARG = peroxisome proliferator-activated receptor,SNP = Single-nucleotide polymorphism,WC = waist circumference,WHR = waist-to-hip ratio,obesity},
mendeley-tags = {obesity},
pages = {293--301},
pmid = {24929207},
title = {{The genetics of human obesity}},
volume = {164},
year = {2014}
}
@article{Kanehisa2000,
author = {Kanehisa, Minoru and Goto, Susumu},
doi = {10.1093/nar/27.1.29},
file = {:home/riku/Documents/Mendeley Desktop/Kanehisa, Goto/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{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 = {:home/riku/Documents/Mendeley Desktop/Gilbert, Slingerland/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}
}
@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 = {:home/riku/Documents/Mendeley Desktop/Jard{\'{e}} et al/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{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 = {:home/riku/Documents/Mendeley Desktop/Gelber et al/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}
}
@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 = {:home/riku/Documents/Mendeley Desktop/Lawrence et al/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{Mckeown1994,
author = {McKeown-Eyssen, Gail},
file = {:home/riku/Documents/Mendeley Desktop/McKeown-Eyssen/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{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 = {:home/riku/Documents/Mendeley Desktop/Khatri, Sirota, Butte/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{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 = {:home/riku/Documents/Mendeley Desktop/Alexandrov et al/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{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 = {:home/riku/Documents/Mendeley Desktop/Lim et al/Lim et al.{\_}2012{\_}A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters i.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{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 = {:home/riku/Documents/Mendeley Desktop/Chang et al/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}
}
@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 = {:home/riku/Documents/Mendeley Desktop/Montague et al/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{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 = {:home/riku/Documents/Mendeley Desktop/Jackson et al/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{Lagergren1999,
author = {Lagergren, Jesper},
doi = {10.7326/0003-4819-130-11-199906010-00003},
file = {:home/riku/Documents/Mendeley Desktop/Lagergren/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{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 = {:home/riku/Documents/Mendeley Desktop/Saxena/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{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 = {:home/riku/Documents/Mendeley Desktop/Huang, Sherman, Lempicki/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{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 = {:home/riku/Documents/Mendeley Desktop/Goeman, B{\"{u}}hlmann/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{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 = {:home/riku/Documents/Mendeley Desktop/Tarca, Bhatti, Romero/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{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 = {:home/riku/Documents/Mendeley Desktop/Hurd, Nelson/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{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 = {:home/riku/Documents/Mendeley Desktop/Pate et al/Pate et al.{\_}1995{\_}Physical activity and public health A recommendation from the Centers for Disease Control and prevention and the Americ.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}
}

license: MIT

license_type: permissive

branch_name: refs/heads/master

extension: bib


text:
SRC_URI = "http://64.34.161.181/download/1.5.0/sources/${P}.tar.gz"
inherit autotools
S = "${WORKDIR}/${PN}"

SRC_URI[md5sum] = "cbfb081fbc4b7fe52f723ab503c328ca"
SRC_URI[sha256sum] = "cf1d47b027d47d151782e93cf67fa6177da5cbe9aded27ab116240d56527c2ba"

repository: overo/overo-oe-natty

repo_name: overo/overo-oe-natty

branch_name: HEAD

extension: bb


text:
@article{Jasiak-2021-Evaluating,
    title = "Evaluating spatiotemporal patterns of arsenic, antimony, and lead deposition from legacy gold mine emissions using lake sediment records",
    author = "Jasiak, Izabela  and
      Wiklund, J.A.  and
      Leclerc, E.  and
      Telford, J.V.  and
      Couture, R.M.  and
      Venkiteswaran, J.J.  and
      Hall, R.I.  and
      Wolfe, B.B.",
    journal = "Applied Geochemistry, Volume 134",
    volume = "134",
    year = "2021",
    publisher = "Elsevier BV",
    url = "https://aclanthology.org/G21-15001",
    doi = "10.1016/j.apgeochem.2021.105053",
    pages = "105053",
}

repository: gwf-uwaterloo/gwf-publications

repo_name: gwf-uwaterloo/gwf-publications

branch_name: refs/heads/main

gha_language: Python


text:
package main

import "Golang-Design-Pattern/Behavioral/Visitor"

func main() {
	//Factory.Test()

	//Singleton.Test()

	//Prototype.Test()

	//Builder.Test()

	//ObjectPool.Test()

	//Adapter.Test()

	//Bridge.Test()

	//Composite.Test()

	//Decorator.Test()

	//Proxy.Test()

	//Flyweight.Test()

	//Facade.Test()

	//Filter.Test()

	//ChainOfResponsibility.Test()

	//Command.Test()

	//Interpreter.Test()

	//Iterator.Test()

	//Iterator.Test2()

	//Iterator.Test3()

	//Mediator.Test()

	//Memento.Test()

	//Observer.Test()

	//State.Test()

	//Strategy.Test()

	Visitor.Test()
}

extension: go