2,033 results on '"Zeleniuch-Jacquotte, A"'
Search Results
202. Inherited variants at 3q13.33 and 3p24.1 are associated with risk of diffuse large B-cell lymphoma and implicate immune pathways
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Qing Lan, Alexandra Nieters, Mark P. Purdue, Christine F. Skibola, Lauren R. Teras, Angela Brooks-Wilson, Kenneth Offit, Anne Zeleniuch-Jacquotte, Joseph Vijai, Simon Crouch, Vivekananda Sarangi, Graham G. Giles, James R. Cerhan, Sophia S. Wang, Nathaniel Rothman, James McKay, Mads Melbye, Karin E. Smedby, Yan W. Asmann, Xifeng Wu, Pierluigi Cocco, Gilles Salles, Hervé Ghesquières, Rebecca D. Jackson, Peter Kraft, Brenda M. Birmann, Huihuang Yan, Sonja I. Berndt, Stephen J. Chanock, Claire M. Vajdic, Demetrius Albanes, Michelle A.T. Hildebrandt, Susan L. Slager, Yuanqing Ye, Geffen Kleinstern, Alain Monnereau, Yawei Zhang, and Roel Vermeulen
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Linkage disequilibrium ,Lymphoma, B-Cell ,Genotype ,Receptors, Cell Surface ,Genome-wide association study ,Single-nucleotide polymorphism ,Locus (genetics) ,Biology ,Polymorphism, Single Nucleotide ,Linkage Disequilibrium ,Article ,03 medical and health sciences ,0302 clinical medicine ,Gene Frequency ,Odds Ratio ,Genetics ,medicine ,Genetic predisposition ,Humans ,SNP ,Genetic Predisposition to Disease ,Promoter Regions, Genetic ,Molecular Biology ,Genetics (clinical) ,030304 developmental biology ,0303 health sciences ,General Medicine ,medicine.disease ,Minor allele frequency ,030220 oncology & carcinogenesis ,B7-2 Antigen ,Chromosomes, Human, Pair 3 ,Diffuse large B-cell lymphoma ,Genome-Wide Association Study - Abstract
We previously identified five single nucleotide polymorphisms (SNPs) at four susceptibility loci for diffuse large B-cell lymphoma (DLBCL) in individuals of European ancestry through a large genome-wide association study (GWAS). To further elucidate genetic susceptibility to DLBCL, we sought to validate two loci at 3q13.33 and 3p24.1 that were suggestive in the original GWAS with additional genotyping. In the meta-analysis (5662 cases and 9237 controls) of the four original GWAS discovery scans and three replication studies, the 3q13.33 locus (rs9831894; minor allele frequency [MAF] = 0.40) was associated with DLBCL risk [odds ratio (OR) = 0.83, P = 3.62 × 10−13]. rs9831894 is in linkage disequilibrium (LD) with additional variants that are part of a super-enhancer that physically interacts with promoters of CD86 and ILDR1. In the meta-analysis (5510 cases and 12 817 controls) of the four GWAS discovery scans and four replication studies, the 3p24.1 locus (rs6773363; MAF = 0.45) was also associated with DLBCL risk (OR = 1.20, P = 2.31 × 10−12). This SNP is 29 426-bp upstream of the nearest gene EOMES and in LD with additional SNPs that are part of a highly lineage-specific and tumor-acquired super-enhancer that shows long-range interaction with AZI2 promoter. These loci provide additional evidence for the role of immune function in the etiology of DLBCL, the most common lymphoma subtype.
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- 2019
203. Anthropometric Risk Factors for Cancers of the Biliary Tract in the Biliary Tract Cancers Pooling Project
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Jessica L. Petrick, Graham G. Giles, Alicja Wolk, Neal D. Freedman, Amy Berrington de Gonzalez, Shoichiro Tsugane, Hans-Olov Adami, Stephanie J. Weinstein, Howard D. Sesso, Jian-Min Yuan, Juhua Luo, Mark P. Purdue, Synnove F. Knutsen, Elisabete Weiderpass, Alison L. Van Dyke, Patricia Hartge, Ruth M. Pfeiffer, Francine Grodstein, Marian L. Neuhouser, Woon-Puay Koh, Renwei Wang, Yu-Tang Gao, Emma E. McGee, Dale P. Sandler, Julie E. Buring, Gary E. Fraser, Katherine A. McGlynn, Rachael Z. Stolzenberg-Solomon, I-Min Lee, Tracey G. Simon, Rashmi Sinha, Kristine R. Monroe, Mazda Jenab, Norie Sawada, Susan M. Gapstur, Catherine Schairer, Linda M. Liao, Susanna C. Larsson, Emily White, Yu Chen, Peter T. Campbell, Anne Zeleniuch-Jacquotte, Jill Koshiol, J. Michael Gaziano, Xuehong Zhang, Sarah S. Jackson, Kim Robien, Bin Zhu, Gabriella Andreotti, Andrew T. Chan, Laura E. Beane Freeman, Jenny N. Poynter, Roger L. Milne, Katie M. O'Brien, Eric J. Grant, Ulrike Peters, Cari M. Kitahara, and Demetrius Albanes
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Male ,0301 basic medicine ,Cancer Research ,medicine.medical_specialty ,Population ,Gastroenterology ,Article ,03 medical and health sciences ,0302 clinical medicine ,Risk Factors ,Internal medicine ,medicine ,Humans ,Prospective Studies ,Gallbladder cancer ,education ,Prospective cohort study ,Biliary tract neoplasm ,education.field_of_study ,Anthropometry ,Proportional hazards model ,business.industry ,Gallbladder ,Middle Aged ,medicine.disease ,Biliary Tract Neoplasms ,030104 developmental biology ,medicine.anatomical_structure ,Oncology ,Biliary tract ,030220 oncology & carcinogenesis ,Female ,business ,Body mass index - Abstract
Biliary tract cancers are rare but highly fatal with poorly understood etiology. Identifying potentially modifiable risk factors for these cancers is essential for prevention. Here we estimated the relationship between adiposity and cancer across the biliary tract, including cancers of the gallbladder (GBC), intrahepatic bile ducts (IHBDC), extrahepatic bile ducts (EHBDC), and the ampulla of Vater (AVC). We pooled data from 27 prospective cohorts with over 2.7 million adults. Adiposity was measured using baseline body mass index (BMI), waist circumference, hip circumference, waist-to-hip, and waist-to-height ratios. HRs and 95% confidence intervals (95% CI) were estimated using Cox proportional hazards models adjusted for sex, education, race, smoking, and alcohol consumption with age as the time metric and the baseline hazard stratified by study. During 37,883,648 person-years of follow-up, 1,343 GBC cases, 1,194 EHBDC cases, 784 IHBDC cases, and 623 AVC cases occurred. For each 5 kg/m2 increase in BMI, there were risk increases for GBC (HR = 1.27; 95% CI, 1.19–1.36), IHBDC (HR = 1.32; 95% CI, 1.21–1.45), and EHBDC (HR = 1.13; 95% CI, 1.03–1.23), but not AVC (HR = 0.99; 95% CI, 0.88–1.11). Increasing waist circumference, hip circumference, waist-to-hip ratio, and waist-to-height ratio were associated with GBC and IHBDC but not EHBDC or AVC. These results indicate that adult adiposity is associated with an increased risk of biliary tract cancer, particularly GBC and IHBDC. Moreover, they provide evidence for recommending weight maintenance programs to reduce the risk of developing these cancers. Significance: These findings identify a correlation between adiposity and biliary tract cancers, indicating that weight management programs may help minimize the risk of these diseases.
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- 2019
204. Development of a Neighborhood Walkability Index for Studying Neighborhood Physical Activity Contexts in Communities across the U.S. over the Past Three Decades
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Michael D. M. Bader, James W. Quinn, Neloufar Rahai, Andrew Rundle, Kathryn M. Neckerman, Gina S. Lovasi, Stephen J. Mooney, Anne Zeleniuch-Jacquotte, Yu Chen, and Katherine Bartley
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Adult ,Male ,medicine.medical_specialty ,Health (social science) ,Poison control ,Walking ,Article ,Occupational safety and health ,Residence Characteristics ,Surveys and Questionnaires ,medicine ,Humans ,Mass index ,Exercise ,Built environment ,Aged ,Public health ,Public Health, Environmental and Occupational Health ,Middle Aged ,United States ,Urban Studies ,Geography ,Walkability ,Environment Design ,Female ,Body mass index ,Forecasting ,Demography ,Cohort study - Abstract
To examine how urban form shapes physical activity and health over time, a measure of neighborhood walkability is needed that can be linked to cohort studies with participants living across the United States (U.S.) that have been followed over the past decades. The Built Environment and Health-Neighborhood Walkability Index (BEH-NWI), a measure of neighborhood walkability that can be calculated for communities across the United States between 1990 and 2015, was conceptualized, developed, and tested using data from the New York City Tri-State Area. BEH-NWI measures were created for 1990 and 2010 using historical data on population density, street intersection density, density of rail stops, and density of pedestrian trip generating/supporting establishments. BEH-NWI scores were calculated for 1-km buffers around the 1990 residences of NYU Women’s Health Study (NYUWHS) participants and NYC Department of Health and Mental Hygiene’s Physical Activity and Transit (PAT) survey participants enrolled in 2011. Higher neighborhood BEH-NWI scores were significantly associated with greater self-reported walking per week (+ 0.31 MET-hours/week per unit BEH-NWI, 95% CI 0.23, 0.36) and lower body mass index (− 0.17 BMI units per unit BEH-NWI, 95% − 0.23, − 0.12) among NYUWHS participants. Higher neighborhood BEH-NWI scores were associated with significantly higher accelerometer-measured physical activity among PAT survey participants (39% more minutes of moderate-intensity equivalent activity/week across the interquartile range of BEH-NWI, 95% CI 21%, 60%). The BEH-NWI can be calculated using historical data going back to 1990, and BEH-NWI scores predict BMI, weekly walking, and physical activity in two NYC area datasets. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s11524-019-00370-4) contains supplementary material, which is available to authorized users.
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- 2019
205. Abstract P1-08-01: Withdrawn
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Katie M. O'Brien, W.-P. Koh, Elisabete Weiderpass, T E Rohan, Kimberly A. Bertrand, Walter C. Willett, J.-M. Yuan, H. O. Adami, Timothy J. Key, Victoria A. Kirsh, M. C. Boutron-Ruault, M. Dorronsoro, Giovanna Masala, RL Milne, Antonia Trichopoulou, Rudolph Kaaks, Dale P. Sandler, Atsuko Sadakane, E. Riboli, Susan E. Hankinson, Minouk J. Schoemaker, Linet, Laure Dossus, Anthony J. Swerdlow, AH Eliassen, Michael Jones, Hazel B. Nichols, Mark N. Brook, Laura Baglietto, Leslie R. Bernstein, Huiyan Ma, Melissa A. Merritt, Malin Sund, Rulla M. Tamimi, Susanna C. Larsson, LB Wright, Cari M. Kitahara, Alicja Wolk, G.G. Giles, Avonne E. Connor, Kotaro Ozasa, Anne Zeleniuch-Jacquotte, Yunn-Yi Chen, C. H. van Gils, Inger T. Gram, Julie R. Palmer, Giske Ursin, Kim Overvad, and K Visvanathan
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Cancer Research ,Oncology - Abstract
This abstract was withdrawn by the authors. Citation Format: Schoemaker MJ, Nichols HB, Wright LB, Brook MN, Jones ME, O'Brien KM, Adami H-O, Baglietto L, Bernstein L, Bertrand KA, Boutron-Ruault M-C, Chen Y, Connor AE, Dorronsoro M, Dossus L, Eliassen AH, Giles GG, Gram IT, Hankinson SE, Kaaks R, Key TJ, Kirsh VA, Kitahara CM, Koh W-P, Larsson SC, Linet MS, Ma H, Masala G, Merritt MA, Milne RL, Overvad K, Ozasa K, Palmer JR, Riboli E, Rohan TE, Sadakane A, Sund M, Tamimi RM, Trichopoulou A, Ursin G, Van Gils CH, Visvanathan K, Weiderpass E, Willett WC, Wolk A, Yuan J-M, Zeleniuch-Jacquotte A, Sandler DP, Swerdlow AJ. Withdrawn [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr P1-08-01.
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- 2019
206. Is high vitamin B12 status a cause of lung cancer?
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Alan A. Arslan, Woon-Puay Koh, Ben Michael Brumpton, Stig E. Bojesen, Mark P. Purdue, Neil E. Caporaso, William J. Blot, Yong-Bing Xiang, Allison M. Hodge, Meir J. Stampfer, Jonas Manjer, Tricia L Larose, I-Min Lee, Gianluca Severi, Robert Carreras-Torres, Rayjean J. Hung, Mikael Johansson, J. Michael Gaziano, Julie E. Buring, Christopher A. Haiman, Per Magne Ueland, S. M. Arnold, Paul Brennan, Qing Lan, Qiuyin Cai, Honglan Li, Howard D. Sesso, Renwei Wang, Kala Visvanathan, Loic Le Marchand, Ulrika Ericson, Edward Giovannucci, Ross L. Prentice, Anouar Fanidi, Christopher I. Amos, Yu-Tang Gao, Demetrius Albanes, Judith Hoffman-Bolton, Xiao-Ou Shu, Caroline L Relton, Stephanie A. Smith-Warner, Mattias Johansson, Jian-Min Yuan, Graham G. Giles, Wei Zheng, Stephanie J. Weinstein, Arnulf Langhammer, Kjell Grankvist, Anne Zeleniuch-Jacquotte, Xuehong Zhang, Neal D. Freedman, Lynne R. Wilkens, Victoria L. Stevens, Øivind Midttun, Mary Pettinger, and Marjorie L. McCullough
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Adult ,Male ,Cancer Research ,medicine.medical_specialty ,Lung Neoplasms ,Single-nucleotide polymorphism ,Polymorphism, Single Nucleotide ,Gastroenterology ,Article ,03 medical and health sciences ,0302 clinical medicine ,Internal medicine ,Mendelian randomization ,Humans ,Medicine ,Prospective Studies ,Vitamin B12 ,Lung cancer ,Aged ,business.industry ,Smoking ,Odds ratio ,Mendelian Randomization Analysis ,Middle Aged ,medicine.disease ,Confidence interval ,Vitamin B 12 ,lung cancer ,Oncology ,Case-Control Studies ,030220 oncology & carcinogenesis ,Etiology ,Biomarker (medicine) ,Female ,ICEP ,business - Abstract
Vitamin B supplementation can have side effects for human health, including cancer risk. We aimed to elucidate the role of vitamin B12 in lung cancer aetiology via direct measurements of pre‐diagnostic circulating vitamin B12 concentrations in a nested case‐control study, complemented with a Mendelian randomization (MR) approach in an independent case‐control sample. We used pre‐diagnostic biomarker data from 5,183 case‐control pairs nested within 20 prospective cohorts, and genetic data from 29,266 cases and 56,450 controls.Exposures included directly measured circulating vitamin B12 in pre‐diagnostic blood samples from the nested case‐control study, and 8 single nucleotide polymorphisms associated with vitamin B12 concentrations in the MR study.Our main outcome of interest was increased risk for lung cancer, overall and by histological subtype, per increase in circulating vitamin B12 concentrations.We found circulating vitamin B12 to be positively associated with overall lung cancer risk in a dose response fashion (odds ratio for a doubling in B12 [ORlog2B12] = 1.15, 95% confidence interval (95%CI) = 1.06‐1.25). The MR analysis based on 8 genetic variants also indicated that genetically determined higher vitamin B12 concentrations were positively associated with overall lung cancer risk (OR per 150 pmol/L standard deviation increase in B12 [ORSD]= 1.08, 95%CI= 1.00‐1.16).Considering the consistency of these two independent and complementary analyses, these findings support the hypothesis that high vitamin B12 status increases the risk of lung cancer.
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- 2019
207. Genome-wide association study of anti-Müllerian hormone levels in pre-menopausal women of late reproductive age and relationship with genetic determinants of reproductive lifespan
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Minouk J. Schoemaker, Ana Luiza Gonçalves Soares, Anne Zeleniuch-Jacquotte, Anthony J. Swerdlow, Michael Jones, A. Heather Eliassen, Anna Murray, Hazel B. Nichols, Jack A. Taylor, Maria Carolina Borges, Dale P. Sandler, Katherine S. Ruth, Peter Kraft, Susan E. Hankinson, and Debbie A Lawlor
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Anti-Mullerian Hormone ,0301 basic medicine ,endocrine system diseases ,menopause ,Gene Expression ,Physiology ,Genome-wide association study ,alles ,0302 clinical medicine ,Ovarian Follicle ,genetics ,genes ,Association Studies Article ,Genetics (clinical) ,0303 health sciences ,030219 obstetrics & reproductive medicine ,mullerian-inhibiting hormone ,adult ,Reproduction ,Age Factors ,Anti-Müllerian hormone ,General Medicine ,Middle Aged ,female genital diseases and pregnancy complications ,Mitochondria ,Menopause ,fetus ,medicine.anatomical_structure ,030220 oncology & carcinogenesis ,Menarche ,sex differentiation ,Female ,life span ,Adult ,endocrine system ,Longevity ,Ovary ,Biology ,Polymorphism, Single Nucleotide ,03 medical and health sciences ,Genetic variation ,ovarian research ,Genetics ,medicine ,oocytes ,Humans ,Allele ,Ovarian reserve ,genome ,Molecular Biology ,Genetic Association Studies ,030304 developmental biology ,Sexual differentiation ,genome-wide association study ,hormones ,Base Sequence ,urogenital system ,menarche ,phlebotomy ,Genetic Variation ,Sequence Analysis, DNA ,medicine.disease ,reproductive physiological process ,ovarian follicle ,030104 developmental biology ,Gene Expression Regulation ,Haplotypes ,Premenopause ,adolescent ,biology.protein ,Transcriptome ,Genome-Wide Association Study - Abstract
Anti-Müllerian hormone (AMH) is required for sexual differentiation in the fetus, and in adult females AMH is produced by growing ovarian follicles. Consequently, AMH levels are correlated with ovarian reserve, declining towards menopause when the oocyte pool is exhausted. A previous genome-wide association study identified three genetic variants in and around the AMH gene that explained 25% of variation in AMH levels in adolescent males but did not identify any genetic associations reaching genome-wide significance in adolescent females. To explore the role of genetic variation in determining AMH levels in women of late reproductive age, we carried out a genome-wide meta-analysis in 3,344 pre-menopausal women from five cohorts (median age 44–48 years at blood draw). A single genetic variant, rs16991615, previously associated with age at menopause, reached genome-wide significance at P=3.48×10−10, with a per allele difference in age-adjusted inverse normal AMH of 0.26 SD (95% CI [0.18,0.34]). We investigated whether genetic determinants of female reproductive lifespan were more generally associated with pre-menopausal AMH levels. Genetically-predicted age at menarche had no robust association but genetically-predicted age at menopause was associated with lower AMH levels by 0.18 SD (95% CI [0.14,0.21]) in age-adjusted inverse normal AMH per one-year earlier age at menopause. Our findings support the hypothesis that AMH is a valid measure of ovarian reserve in pre-menopausal women and suggest that the underlying biology of ovarian reserve results in a causal link between pre-menopausal AMH levels and menopause timing.
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- 2019
208. Further Confirmation of Germline Glioma Risk Variant rs78378222 in TP53 and Its Implication in Tumor Tissues via Integrative Analysis of TCGA Data
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Wang, Zhaoming, Rajaraman, Preetha, Melin, Beatrice S., Chung, Charles C., Zhang, Weijia, McKean-Cowdin, Roberta, Michaud, Dominique, Yeager, Meredith, Ahlbom, Anders, Albanes, Demetrius, Andersson, Ulrika, Freeman, Laura Beane E., Buring, Julie E., Butler, Mary Ann, Carreón, Tania, Feychting, Maria, Gapstur, Susan M., Gaziano, Michael J., Giles, Graham G., Hallmans, Goran, Henriksson, Roger, Hoffman-Bolton, Judith, Inskip, Peter D., Kitahara, Cari M., Le Marchand, Loic, Linet, Martha S., Li, Shengchao, Peters, Ulrike, Purdue, Mark P., Rothman, Nathaniel, Ruder, Avima M., Sesso, Howard D., Severi, Gianluca, Stampfer, Meir, Stevens, Victoria L., Visvanathan, Kala, Wang, Sophia S., White, Emily, Zeleniuch-Jacquotte, Anne, Hoover, Robert, Fraumeni, Joseph F., Chatterjee, Nilanjan, Hartge, Patricia, and Chanock, Stephen J.
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- 2015
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209. Intrauterine devices and endometrial cancer risk: A pooled analysis of the Epidemiology of Endometrial Cancer Consortium
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Felix, Ashley S., Gaudet, Mia M., Vecchia, Carlo La, Nagle, Christina M., Shu, Xiao Ou, Weiderpass, Elisabete, Adami, Hans Olov, Beresford, Shirley, Bernstein, Leslie, Chen, Chu, Cook, Linda S., Vivo, Immaculata De, Doherty, Jennifer A., Friedenreich, Christine M., Gapstur, Susan M., Hill, Dierdre, Horn-Ross, Pamela L., Lacey, James V., Levi, Fabio, Liang, Xiaolin, Lu, Lingeng, Magliocco, Anthony, McCann, Susan E., Negri, Eva, Olson, Sara H., Palmer, Julie R., Patel, Alpa V., Petruzella, Stacey, Prescott, Jennifer, Risch, Harvey A., Rosenberg, Lynn, Sherman, Mark E., Spurdle, Amanda B., Webb, Penelope M., Wise, Lauren A., Xiang, Yong-Bing, Xu, Wanghong, Yang, Hannah P., Yu, Herbert, Zeleniuch-Jacquotte, Anne, and Brinton, Louise A.
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- 2015
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210. Association between class III obesity (BMI of 40-59 kg/m2) and mortality: a pooled analysis of 20 prospective studies.
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Cari M Kitahara, Alan J Flint, Amy Berrington de Gonzalez, Leslie Bernstein, Michelle Brotzman, Robert J MacInnis, Steven C Moore, Kim Robien, Philip S Rosenberg, Pramil N Singh, Elisabete Weiderpass, Hans Olov Adami, Hoda Anton-Culver, Rachel Ballard-Barbash, Julie E Buring, D Michal Freedman, Gary E Fraser, Laura E Beane Freeman, Susan M Gapstur, John Michael Gaziano, Graham G Giles, Niclas Håkansson, Jane A Hoppin, Frank B Hu, Karen Koenig, Martha S Linet, Yikyung Park, Alpa V Patel, Mark P Purdue, Catherine Schairer, Howard D Sesso, Kala Visvanathan, Emily White, Alicja Wolk, Anne Zeleniuch-Jacquotte, and Patricia Hartge
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Medicine - Abstract
The prevalence of class III obesity (body mass index [BMI]≥40 kg/m2) has increased dramatically in several countries and currently affects 6% of adults in the US, with uncertain impact on the risks of illness and death. Using data from a large pooled study, we evaluated the risk of death, overall and due to a wide range of causes, and years of life expectancy lost associated with class III obesity.In a pooled analysis of 20 prospective studies from the United States, Sweden, and Australia, we estimated sex- and age-adjusted total and cause-specific mortality rates (deaths per 100,000 persons per year) and multivariable-adjusted hazard ratios for adults, aged 19-83 y at baseline, classified as obese class III (BMI 40.0-59.9 kg/m2) compared with those classified as normal weight (BMI 18.5-24.9 kg/m2). Participants reporting ever smoking cigarettes or a history of chronic disease (heart disease, cancer, stroke, or emphysema) on baseline questionnaires were excluded. Among 9,564 class III obesity participants, mortality rates were 856.0 in men and 663.0 in women during the study period (1976-2009). Among 304,011 normal-weight participants, rates were 346.7 and 280.5 in men and women, respectively. Deaths from heart disease contributed largely to the excess rates in the class III obesity group (rate differences = 238.9 and 132.8 in men and women, respectively), followed by deaths from cancer (rate differences = 36.7 and 62.3 in men and women, respectively) and diabetes (rate differences = 51.2 and 29.2 in men and women, respectively). Within the class III obesity range, multivariable-adjusted hazard ratios for total deaths and deaths due to heart disease, cancer, diabetes, nephritis/nephrotic syndrome/nephrosis, chronic lower respiratory disease, and influenza/pneumonia increased with increasing BMI. Compared with normal-weight BMI, a BMI of 40-44.9, 45-49.9, 50-54.9, and 55-59.9 kg/m2 was associated with an estimated 6.5 (95% CI: 5.7-7.3), 8.9 (95% CI: 7.4-10.4), 9.8 (95% CI: 7.4-12.2), and 13.7 (95% CI: 10.5-16.9) y of life lost. A limitation was that BMI was mainly ascertained by self-report.Class III obesity is associated with substantially elevated rates of total mortality, with most of the excess deaths due to heart disease, cancer, and diabetes, and major reductions in life expectancy compared with normal weight. Please see later in the article for the Editors' Summary.
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- 2014
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211. Agnostic Pathway/Gene Set Analysis of Genome-Wide Association Data Identifies Associations for Pancreatic Cancer
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Paula L. Hyland, Sonja I. Berndt, Michelle Cotterchio, Rayjean J. Hung, Stephen K. Van Den Eeden, Núria Malats, Sara H. Olson, Rachel E. Neale, Eric A. Klein, Gloria M. Petersen, Eric J. Duell, Ann L. Oberg, Naomi Walsh, Robert C. Kurtz, Kari G Chaffee, Anne Zeleniuch-Jacquotte, Elisabete Weiderpass, Elizabeth A Holly, Brian M. Wolpin, Vladimir Janout, Lauren K. Brais, Paul Brennan, Qi Yang, Federico Canzian, Patricia Hartge, Han Zhang, Irene Collins, Peter Kraft, S. Chanock, Satu Männistö, PanScan, Christopher A. Haiman, Erica J. Childs, Wei Zheng, Robert N. Hoover, Malin Sund, Ayelet Borgida, Joseph M. Herman, Rachael Z. Stolzenberg-Solomon, Harvey A. Risch, Gabriella Andreotti, Oliver Strobel, Julie E. Buring, Kala Visvanathan, Ivana Holcatova, Nicholas J. Wareham, Paige M. Bracci, Nathaniel Rothman, Zhaoming Wang, Alison P Klein, Howard D. Sesso, Graham G. Giles, Gary E. Goodman, Edward Giovannucci, Michael Goggins, Emily White, Demetrius Albanes, Phyllis J. Goodman, Sean Cleary, Roger L. Milne, Francisco X. Real, Kathy J. Helzlsouer, Miquel Porta, Charles S. Fuchs, B. Bueno-de-Mesquita, Thilo Hackert, Lingeng Lu, Ghislaine Scelo, Marie-Christine Boutron-Ruault, Ana Babic, Herbert Yu, Laura Beane-Freeman, PanC consortia, J. Michael Gaziano, Laufey T. Amundadottir, Mark D Thornquist, I-Min Lee, Ulrike Peters, Mingfeng Zhang, Donghui Li, Eric J. Jacobs, Evelina Mocci, William Wheeler, Kai Yu, William R. Bamlet, Gianluca Severi, Xiao O. Shu, Alpa V. Patel, Alan A. Arslan, Charles Kooperberg, D. Silverman, Daniel Laheru, Irene Orlow, Steven Gallinger, J. Wactawski-Wende, Geoffrey S Tobias, Loic LeMarchand, Nicolas Wentzensen, Lenka Foretová, Manal Hasan, and Department of Medical and Clinical Genetics
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EXPRESSION ,Developmental genetics ,Cancer Research ,GENES ,SUSCEPTIBILITY LOCI ,Pàncrees -- Genètica ,3122 Cancers ,Genome-wide association study ,Single-nucleotide polymorphism ,Computational biology ,VARIANTS ,Biology ,Polymorphism, Single Nucleotide ,Genome ,03 medical and health sciences ,Pàncrees -- Malalties ,0302 clinical medicine ,Pancreatic cancer ,ENDOTHELIN ,medicine ,Humans ,BREAST-CANCER ,Genetic Predisposition to Disease ,TRANSCRIPTOME ,Gene ,Càncer de pàncrees ,Pancreas cancer ,Pàncrees -- Càncer ,Genetic association ,Models, Statistical ,RECEPTOR ,MUTATIONS ,Case-control study ,Articles ,medicine.disease ,3. Good health ,Pancreatic Neoplasms ,Oncology ,Case-Control Studies ,030220 oncology & carcinogenesis ,Meta-analysis ,METASTASIS ,Carcinoma, Pancreatic Ductal ,Genome-Wide Association Study ,Genètica del desenvolupament - Abstract
Background: Genome-wide association studies (GWAS) identify associations of individual single-nucleotide polymorphisms (SNPs) with cancer risk but usually only explain a fraction of the inherited variability. Pathway analysis of genetic variants is a powerful tool to identify networks of susceptibility genes. Methods: We conducted a large agnostic pathway-based meta-analysis of GWAS data using the summary-based adaptive rank truncated product method to identify gene sets and pathways associated with pancreatic ductal adenocarcinoma (PDAC) in 9040 cases and 12 496 controls. We performed expression quantitative trait loci (eQTL) analysis and functional annotation of the top SNPs in genes contributing to the top associated pathways and gene sets. All statistical tests were two-sided. Results: We identified 14 pathways and gene sets associated with PDAC at a false discovery rate of less than 0.05. After Bonferroni correction (P
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- 2018
212. Reproducibility of serum cytokines and growth factors
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Gu, Yian, Zeleniuch-Jacquotte, Anne, Linkov, Faina, Koenig, Karen L., Liu, Mengling, Velikokhatnaya, Lyudmila, Shore, Roy E., Marrangoni, Adele, Toniolo, Paolo, Lokshin, Anna E., and Arslan, Alan A.
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- 2009
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213. Prediagnostic antibody responses to Fusobacterium nucleatum proteins are not associated with risk of colorectal cancer in a large United States consortium
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Meira Epplein, Lauren R. Teras, Sonja I. Berndt, Sylvia Wassertheil-Smoller, Christopher A. Haiman, William J. Blot, Yu Chen, Loic Le Marchand, Howard D. Sesso, Timothy L. Cover, John D. Potter, Lesley F. Tinker, Chun-Han Lo, Tim Waterboer, Kala Visvanathan, Richard M. Peek, Anne Zeleniuch-Jacquotte, Mingyang Song, and Julia Butt
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Oncology ,Male ,medicine.medical_specialty ,Future studies ,Epidemiology ,Colorectal cancer ,Specific detection ,Immunoglobulin Isotypes ,Risk Assessment ,Article ,stomatognathic system ,Bacterial Proteins ,Seroepidemiologic Studies ,Internal medicine ,medicine ,Seroprevalence ,Humans ,Prospective Studies ,Aged ,biology ,Fusobacterium nucleatum ,business.industry ,Middle Aged ,biology.organism_classification ,medicine.disease ,Antibodies, Bacterial ,United States ,Gastrointestinal Microbiome ,stomatognathic diseases ,Antibody response ,Case-Control Studies ,biology.protein ,Female ,Antibody ,business ,Colorectal Neoplasms - Abstract
Background: The association between prediagnostic antibody responses to Fusobacterium nucleatum (F. nucleatum) and subsequent risk of colorectal cancer is not established. Methods: We conducted a nested case–control study of 8,126 participants in a consortium of 10 prospective cohorts in the United States. Results: Higher seroprevalence of any F. nucleatum antibody was observed among non-White participants (51.1%) compared with White participants (31.2%). We did not find any statistically significant association between seropositivity to any of the eight F. nucleatum proteins and colorectal cancer risk. Conclusions: Prediagnostic antibody responses to F. nucleatum proteins were not associated with the risk of colorectal cancer. Impact: Future studies may consider a more specific detection of the immunoglobulin isotypes or focus on examining F. nucleatum in stool or tissue samples.
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- 2021
214. Breast Cancer Risk Factors and Circulating Anti-Müllerian Hormone Concentration in Healthy Premenopausal Women
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Anne Zeleniuch-Jacquotte, Timothy J. Key, A. Heather Eliassen, Mengling Liu, Karen L. Koenig, Elizabeth R. Bertone-Johnson, Roni T. Falk, Tess V. Clendenen, Judith Hoffman-Bolton, Göran Hallmans, Wenzhen Ge, Anthony J. Swerdlow, Louise A. Brinton, Kala Visvanathan, Claudia Agnoli, Minouk J. Schoemaker, Patrick M. Sluss, Malin Sund, Farbod Darvishian, Vittorio Krogh, Dale P. Sandler, Hazel B. Nichols, Susan E. Hankinson, Joanne F. Dorgan, and Yelena Afanasyeva
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Adult ,Anti-Mullerian Hormone ,medicine.medical_specialty ,endocrine system ,Aging ,Endocrinology, Diabetes and Metabolism ,Clinical Biochemistry ,Population ,Breast Neoplasms ,Biochemistry ,Body Mass Index ,Cohort Studies ,Breast Diseases ,Endocrinology ,Breast cancer ,Pregnancy ,Risk Factors ,Internal medicine ,Medicine ,Humans ,education ,Ovarian Reserve ,Online Only Articles ,education.field_of_study ,biology ,business.industry ,Obstetrics ,Biochemistry (medical) ,Anti-Müllerian hormone ,Middle Aged ,medicine.disease ,Menopause ,Cross-Sectional Studies ,Premenopause ,Risk factors for breast cancer ,biology.protein ,Female ,Breast disease ,business ,Body mass index ,Biomarkers ,Cohort study - Abstract
Context We previously reported that anti-Müllerian hormone (AMH), a marker of ovarian reserve, is positively associated with breast cancer risk, consistent with other studies. Objective This study assessed whether risk factors for breast cancer are correlates of AMH concentration. Methods This cross-sectional study included 3831 healthy premenopausal women (aged 21-57, 87% aged 35-49) from 10 cohort studies among the general population. Results Adjusting for age and cohort, AMH positively associated with age at menarche (P Conclusion This is the largest study of AMH and breast cancer risk factors among women from the general population (not presenting with infertility), and it suggests that most associations are limited to women over 40, who are approaching menopause and whose AMH concentration is declining.
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- 2021
215. Imputation and subset-based association analysis across different cancer types identifies multiple independent risk loci in the TERT-CLPTM1L region on chromosome 5p15.33
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Wang, Zhaoming, Zhu, Bin, Zhang, Mingfeng, Parikh, Hemang, Jia, Jinping, Chung, Charles C., Sampson, Joshua N., Hoskins, Jason W., Hutchinson, Amy, Burdette, Laurie, Ibrahim, Abdisamad, Hautman, Christopher, Raj, Preethi S., Abnet, Christian C., Adjei, Andrew A., Ahlbom, Anders, Albanes, Demetrius, Allen, Naomi E., Ambrosone, Christine B., Aldrich, Melinda, Amiano, Pilar, Amos, Christopher, Andersson, Ulrika, Andriole, Gerald, Jr, Andrulis, Irene L., Arici, Cecilia, Arslan, Alan A., Austin, Melissa A., Baris, Dalsu, Barkauskas, Donald A., Bassig, Bryan A., Beane Freeman, Laura E., Berg, Christine D., Berndt, Sonja I., Bertazzi, Pier Alberto, Biritwum, Richard B., Black, Amanda, Blot, William, Boeing, Heiner, Boffetta, Paolo, Bolton, Kelly, Boutron-Ruault, Marie-Christine, Bracci, Paige M., Brennan, Paul, Brinton, Louise A., Brotzman, Michelle, Bueno-de-Mesquita, H. Bas, Buring, Julie E., Butler, Mary Ann, Cai, Qiuyin, Cancel-Tassin, Geraldine, Canzian, Federico, Cao, Guangwen, Caporaso, Neil E., Carrato, Alfredo, Carreon, Tania, Carta, Angela, Chang, Gee-Chen, Chang, I-Shou, Chang-Claude, Jenny, Che, Xu, Chen, Chien-Jen, Chen, Chih-Yi, Chen, Chung-Hsing, Chen, Constance, Chen, Kuan-Yu, Chen, Yuh-Min, Chokkalingam, Anand P., Chu, Lisa W., Clavel-Chapelon, Francoise, Colditz, Graham A., Colt, Joanne S., Conti, David, Cook, Michael B., Cortessis, Victoria K., Crawford, E. David, Cussenot, Olivier, Davis, Faith G., De Vivo, Immaculata, Deng, Xiang, Ding, Ti, Dinney, Colin P., Di Stefano, Anna Luisa, Diver, W. Ryan, Duell, Eric J., Elena, Joanne W., Fan, Jin-Hu, Feigelson, Heather Spencer, Feychting, Maria, Figueroa, Jonine D., Flanagan, Adrienne M., Fraumeni, Joseph F., Jr, Freedman, Neal D., Fridley, Brooke L., Fuchs, Charles S., Gago-Dominguez, Manuela, Gallinger, Steven, Gao, Yu-Tang, Gapstur, Susan M., Garcia-Closas, Montserrat, Garcia-Closas, Reina, Gastier-Foster, Julie M., Gaziano, J. Michael, Gerhard, Daniela S., Giffen, Carol A., Giles, Graham G., Gillanders, Elizabeth M., Giovannucci, Edward L., Goggins, Michael, Gokgoz, Nalan, Goldstein, Alisa M., Gonzalez, Carlos, Gorlick, Richard, Greene, Mark H., Gross, Myron, Grossman, H. Barton, Grubb, Robert, III, Gu, Jian, Guan, Peng, Haiman, Christopher A., Hallmans, Goran, Hankinson, Susan E., Harris, Curtis C., Hartge, Patricia, Hattinger, Claudia, Hayes, Richard B., He, Qincheng, Helman, Lee, Henderson, Brian E., Henriksson, Roger, Hoffman-Bolton, Judith, Hohensee, Chancellor, Holly, Elizabeth A., Hong, Yun-Chul, Hoover, Robert N., Hosgood, H. Dean, III, Hsiao, Chin-Fu, Hsing, Ann W., Hsiung, Chao Agnes, Hu, Nan, Hu, Wei, Hu, Zhibin, Huang, Ming-Shyan, Hunter, David J., Inskip, Peter D., Ito, Hidemi, Jacobs, Eric J., Jacobs, Kevin B., Jenab, Mazda, Ji, Bu-Tian, Johansen, Christoffer, Johansson, Mattias, Johnson, Alison, Kaaks, Rudolf, Kamat, Ashish M., Kamineni, Aruna, Karagas, Margaret, Khanna, Chand, Khaw, Kay-Tee, Kim, Christopher, Kim, In-Sam, Kim, Jin Hee, Kim, Yeul Hong, Kim, Young-Chul, Kim, Young Tae, Kang, Chang Hyun, Jung, Yoo Jin, Kitahara, Cari M., Klein, Alison P., Klein, Robert, Kogevinas, Manolis, Koh, Woon-Puay, Kohno, Takashi, Kolonel, Laurence N., Kooperberg, Charles, Kratz, Christian P., Krogh, Vittorio, Kunitoh, Hideo, Kurtz, Robert C., Kurucu, Nilgun, Lan, Qing, Lathrop, Mark, Lau, Ching C., Lecanda, Fernando, Lee, Kyoung-Mu, Lee, Maxwell P., Le Marchand, Loic, Lerner, Seth P., Li, Donghui, Liao, Linda M., Lim, Wei-Yen, Lin, Dongxin, Lin, Jie, Lindstrom, Sara, Linet, Martha S., Lissowska, Jolanta, Liu, Jianjun, Ljungberg, Börje, Lloreta, Josep, Lu, Daru, Ma, Jing, Malats, Nuria, Mannisto, Satu, Marina, Neyssa, Mastrangelo, Giuseppe, Matsuo, Keitaro, McGlynn, Katherine A., McKean-Cowdin, Roberta, McNeill, Lorna H., McWilliams, Robert R., Melin, Beatrice S., Meltzer, Paul S., Mensah, James E., Miao, Xiaoping, Michaud, Dominique S., Mondul, Alison M., Moore, Lee E., Muir, Kenneth, Niwa, Shelley, Olson, Sara H., Orr, Nick, Panico, Salvatore, Park, Jae Yong, Patel, Alpa V., Patino-Garcia, Ana, Pavanello, Sofia, Peeters, Petra H. M., Peplonska, Beata, Peters, Ulrike, Petersen, Gloria M., Picci, Piero, Pike, Malcolm C., Porru, Stefano, Prescott, Jennifer, Pu, Xia, Purdue, Mark P., Qiao, You-Lin, Rajaraman, Preetha, Riboli, Elio, Risch, Harvey A., Rodabough, Rebecca J., Rothman, Nathaniel, Ruder, Avima M., Ryu, Jeong-Seon, Sanson, Marc, Schned, Alan, Schumacher, Fredrick R., Schwartz, Ann G., Schwartz, Kendra L., Schwenn, Molly, Scotlandi, Katia, Seow, Adeline, Serra, Consol, Serra, Massimo, Sesso, Howard D., Severi, Gianluca, Shen, Hongbing, Shen, Min, Shete, Sanjay, Shiraishi, Kouya, Shu, Xiao-Ou, Siddiq, Afshan, Sierrasesumaga, Luis, Sierri, Sabina, Loon Sihoe, Alan Dart, Silverman, Debra T., Simon, Matthias, Southey, Melissa C., Spector, Logan, Spitz, Margaret, Stampfer, Meir, Stattin, Par, Stern, Mariana C., Stevens, Victoria L., Stolzenberg-Solomon, Rachael Z., Stram, Daniel O., Strom, Sara S., Su, Wu-Chou, Sund, Malin, Sung, Sook Whan, Swerdlow, Anthony, Tan, Wen, Tanaka, Hideo, Tang, Wei, Tang, Ze-Zhang, Tardon, Adonina, Tay, Evelyn, Taylor, Philip R., Tettey, Yao, Thomas, David M., Tirabosco, Roberto, Tjonneland, Anne, Tobias, Geoffrey S., Toro, Jorge R., Travis, Ruth C., Trichopoulos, Dimitrios, Troisi, Rebecca, Truelove, Ann, Tsai, Ying-Huang, Tucker, Margaret A., Tumino, Rosario, Van Den Berg, David, Van Den Eeden, Stephen K., Vermeulen, Roel, Vineis, Paolo, Visvanathan, Kala, Vogel, Ulla, Wang, Chaoyu, Wang, Chengfeng, Wang, Junwen, Wang, Sophia S., Weiderpass, Elisabete, Weinstein, Stephanie J., Wentzensen, Nicolas, Wheeler, William, White, Emily, Wiencke, John K., Wolk, Alicja, Wolpin, Brian M., Wong, Maria Pik, Wrensch, Margaret, Wu, Chen, Wu, Tangchun, Wu, Xifeng, Wu, Yi-Long, Wunder, Jay S., Xiang, Yong-Bing, Xu, Jun, Yang, Hannah P., Yang, Pan-Chyr, Yatabe, Yasushi, Ye, Yuanqing, Yeboah, Edward D., Yin, Zhihua, Ying, Chen, Yu, Chong-Jen, Yu, Kai, Yuan, Jian-Min, Zanetti, Krista A., Zeleniuch-Jacquotte, Anne, Zheng, Wei, Zhou, Baosen, Mirabello, Lisa, Savage, Sharon A., Kraft, Peter, Chanock, Stephen J., Yeager, Meredith, Landi, Maria Terese, Shi, Jianxin, Chatterjee, Nilanjan, and Amundadottir, Laufey T.
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- 2014
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216. Serum taurine and risk of coronary heart disease: a prospective, nested case–control study
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Wójcik, Oktawia P., Koenig, Karen L., Zeleniuch-Jacquotte, Anne, Pearte, Camille, Costa, Max, and Chen, Yu
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- 2013
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217. Prolactin and Risk of Epithelial Ovarian Cancer
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Hathaway, Cassandra A., primary, Rice, Megan S., additional, Townsend, Mary K., additional, Hankinson, Susan E., additional, Arslan, Alan A., additional, Buring, Julie E., additional, Hallmans, Göran, additional, Idahl, Annika, additional, Kubzansky, Laura D., additional, Lee, I-Min, additional, Lundin, Eva A., additional, Sluss, Patrick M., additional, Zeleniuch-Jacquotte, Anne, additional, and Tworoger, Shelley S., additional
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- 2021
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218. Breast Cancer Risk Factors and Circulating Anti-Müllerian Hormone Concentration in Healthy Premenopausal Women
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Clendenen, Tess V, primary, Ge, Wenzhen, additional, Koenig, Karen L, additional, Afanasyeva, Yelena, additional, Agnoli, Claudia, additional, Bertone-Johnson, Elizabeth, additional, Brinton, Louise A, additional, Darvishian, Farbod, additional, Dorgan, Joanne F, additional, Eliassen, A Heather, additional, Falk, Roni T, additional, Hallmans, Göran, additional, Hankinson, Susan E, additional, Hoffman-Bolton, Judith, additional, Key, Timothy J, additional, Krogh, Vittorio, additional, Nichols, Hazel B, additional, Sandler, Dale P, additional, Schoemaker, Minouk J, additional, Sluss, Patrick M, additional, Sund, Malin, additional, Swerdlow, Anthony J, additional, Visvanathan, Kala, additional, Liu, Mengling, additional, and Zeleniuch-Jacquotte, Anne, additional
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- 2021
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219. Nongenetic Determinants of Risk for Early-Onset Colorectal Cancer
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Archambault, Alexi N, primary, Lin, Yi, additional, Jeon, Jihyoun, additional, Harrison, Tabitha A, additional, Bishop, D Timothy, additional, Brenner, Hermann, additional, Casey, Graham, additional, Chan, Andrew T, additional, Chang-Claude, Jenny, additional, Figueiredo, Jane C, additional, Gallinger, Steven, additional, Gruber, Stephen B, additional, Gunter, Marc J, additional, Hoffmeister, Michael, additional, Jenkins, Mark A, additional, Keku, Temitope O, additional, Marchand, Loïc Le, additional, Li, Li, additional, Moreno, Victor, additional, Newcomb, Polly A, additional, Pai, Rish, additional, Parfrey, Patrick S, additional, Rennert, Gad, additional, Sakoda, Lori C, additional, Sandler, Robert S, additional, Slattery, Martha L, additional, Song, Mingyang, additional, Win, Aung Ko, additional, Woods, Michael O, additional, Murphy, Neil, additional, Campbell, Peter T, additional, Su, Yu-Ru, additional, Zeleniuch-Jacquotte, Anne, additional, Liang, Peter S, additional, Du, Mengmeng, additional, Hsu, Li, additional, Peters, Ulrike, additional, and Hayes, Richard B, additional
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- 2021
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220. Epidemiology of 40 blood biomarkers of one-carbon metabolism, vitamin status, inflammation, and renal and endothelial function among cancer-free older adults
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Woon-Puay Koh, Mattias Johansson, Jian-Min Yuan, Kjell Grankvist, Howard D. Sesso, Demetrius Albanes, Elin Pettersen Sørgjerd, Mikael Johansson, Xiao-Ou Shu, Graham G. Giles, Kala Visvanathan, Loic Le Marchand, Paul Brennan, Malte Sandsveden, Ross L. Prentice, Alan A. Arslan, Qiuyin Cai, Neal D. Freedman, Roger L. Milne, Jonas Manjer, J. Michael Gaziano, Hilary A. Robbins, Lynne R. Wilkens, Victoria L. Stevens, Hana Zahed, Florence Guida, Chu Chen, Wen Yi Huang, Anne Zeleniuch-Jacquotte, Stephanie J. Weinstein, Per Magne Ueland, Arnulf Langhammer, Xuehong Zhang, Wei Zheng, Ying Wang, William J. Blot, Anouar Fanidi, David C. Muller, and Øivind Midttun
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Male ,0301 basic medicine ,Epidemiology ,Science ,medicine.medical_treatment ,Population ,Physiology ,Renal function ,Kidney ,Article ,Body Mass Index ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,medicine ,Humans ,education ,Kynurenine ,Aged ,Aged, 80 and over ,Inflammation ,Creatinine ,education.field_of_study ,Cancer och onkologi ,Multidisciplinary ,business.industry ,Smoking ,Vitamins ,Middle Aged ,Carbon ,B vitamins ,C-Reactive Protein ,030104 developmental biology ,chemistry ,030220 oncology & carcinogenesis ,Cancer and Oncology ,Cohort ,Medicine ,Smoking cessation ,Biomarker (medicine) ,Female ,Smoking Cessation ,business ,Body mass index ,Biomarkers - Abstract
Imbalances of blood biomarkers are associated with disease, and biomarkers may also vary non-pathologically across population groups. We described variation in concentrations of biomarkers of one-carbon metabolism, vitamin status, inflammation including tryptophan metabolism, and endothelial and renal function among cancer-free older adults. We analyzed 5167 cancer-free controls aged 40–80 years from 20 cohorts in the Lung Cancer Cohort Consortium (LC3). Centralized biochemical analyses of 40 biomarkers in plasma or serum were performed. We fit multivariable linear mixed effects models to quantify variation in standardized biomarker log-concentrations across four factors: age, sex, smoking status, and body mass index (BMI). Differences in most biomarkers across most factors were small, with 93% (186/200) of analyses showing an estimated difference lower than 0.25 standard-deviations, although most were statistically significant due to large sample size. The largest difference was for creatinine by sex, which was − 0.91 standard-deviations lower in women than men (95%CI − 0.98; − 0.84). The largest difference by age was for total cysteine (0.40 standard-deviation increase per 10-year increase, 95%CI 0.36; 0.43), and by BMI was for C-reactive protein (0.38 standard-deviation increase per 5-kg/m2 increase, 95%CI 0.34; 0.41). For 31 of 40 markers, the mean difference between current and never smokers was larger than between former and never smokers. A statistically significant (p
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- 2021
221. Body size and weight change over adulthood and risk of breast cancer by menopausal and hormone receptor status : a pooled analysis of 20 prospective cohort studies
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van den Brandt, Piet A, Ziegler, Regina G, Wang, Molin, Hou, Tao, Li, Ruifeng, Adami, Hans-Olov, Agnoli, Claudia, Bernstein, Leslie, Buring, Julie E, Chen, Yu, Connor, Avonne E, Eliassen, A Heather, Genkinger, Jeanine M, Gierach, Gretchen, Giles, Graham G, Goodman, Gary G, Håkansson, Niclas, Krogh, Vittorio, Le Marchand, Loic, Lee, I-Min, Liao, Linda M, Martinez, M Elena, Miller, Anthony B, Milne, Roger L, Neuhouser, Marian L, Patel, Alpa V, Prizment, Anna, Robien, Kim, Rohan, Thomas E, Sawada, Norie, Schouten, Leo J, Sinha, Rashmi, Stolzenberg-Solomon, Rachael Z, Teras, Lauren R, Tsugane, Shoichiro, Visvanathan, Kala, Weiderpass, Elisabete, White, Kami K, Willett, Walter C, Wolk, Alicja, Zeleniuch-Jacquotte, Anne, Smith-Warner, Stephanie A, van den Brandt, Piet A, Ziegler, Regina G, Wang, Molin, Hou, Tao, Li, Ruifeng, Adami, Hans-Olov, Agnoli, Claudia, Bernstein, Leslie, Buring, Julie E, Chen, Yu, Connor, Avonne E, Eliassen, A Heather, Genkinger, Jeanine M, Gierach, Gretchen, Giles, Graham G, Goodman, Gary G, Håkansson, Niclas, Krogh, Vittorio, Le Marchand, Loic, Lee, I-Min, Liao, Linda M, Martinez, M Elena, Miller, Anthony B, Milne, Roger L, Neuhouser, Marian L, Patel, Alpa V, Prizment, Anna, Robien, Kim, Rohan, Thomas E, Sawada, Norie, Schouten, Leo J, Sinha, Rashmi, Stolzenberg-Solomon, Rachael Z, Teras, Lauren R, Tsugane, Shoichiro, Visvanathan, Kala, Weiderpass, Elisabete, White, Kami K, Willett, Walter C, Wolk, Alicja, Zeleniuch-Jacquotte, Anne, and Smith-Warner, Stephanie A
- Abstract
Associations between anthropometric factors and breast cancer (BC) risk have varied inconsistently by estrogen and/or progesterone receptor (ER/PR) status. Associations between prediagnostic anthropometric factors and risk of premenopausal and postmenopausal BC overall and ER/PR status subtypes were investigated in a pooled analysis of 20 prospective cohorts, including 36,297 BC cases among 1,061,915 women, using multivariable Cox regression analyses, controlling for reproductive factors, diet and other risk factors. We estimated dose-response relationships and tested for nonlinear associations using restricted cubic splines. Height showed positive, linear associations for premenopausal and postmenopausal BC risk (6-7% RR increase per 5 cm increment), with stronger associations for receptor-positive subtypes. Body mass index (BMI) at cohort baseline was strongly inversely associated with premenopausal BC risk, and strongly positively-and nonlinearly-associated with postmenopausal BC (especially among women who never used hormone replacement therapy). This was primarily observed for receptor-positive subtypes. Early adult BMI (at 18-20 years) showed inverse, linear associations for premenopausal and postmenopausal BC risk (21% and 11% RR decrease per 5 kg/m2, respectively) with stronger associations for receptor-negative subtypes. Adult weight gain since 18-20 years was positively associated with postmenopausal BC risk, stronger for receptor-positive subtypes, and among women who were leaner in early adulthood. Women heavier in early adulthood generally had reduced premenopausal BC risk, independent of later weight gain. Positive associations between height, baseline (adult) BMI, adult weight gain and postmenopausal BC risk were substantially stronger for hormone receptor-positive versus negative subtypes. Premenopausal BC risk was positively associated with height, but inversely with baseline BMI and weight gain (mostly in receptor-positive subtypes). Inverse associ
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- 2021
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222. Epidemiology of 40 blood biomarkers of one-carbon metabolism, vitamin status, inflammation, and renal and endothelial function among cancer-free older adults.
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Zahed H., Ueland P.M., Midttun O., Milne R.L., Giles G.G., Manjer J., Sandsveden M., Langhammer A., Sorgjerd E.P., Grankvist K., Johansson M., Freedman N.D., Huang W.-Y., Chen C., Prentice R., Stevens V.L., Wang Y., Le Marchand L., Wilkens L.R., Weinstein S.J., Albanes D., Cai Q., Blot W.J., Arslan A.A., Zeleniuch-Jacquotte A., Shu X.-O., Zheng W., Yuan J.-M., Koh W.-P., Visvanathan K., Sesso H.D., Zhang X., Gaziano J.M., Fanidi A., Muller D., Brennan P., Guida F., Robbins H.A., Zahed H., Ueland P.M., Midttun O., Milne R.L., Giles G.G., Manjer J., Sandsveden M., Langhammer A., Sorgjerd E.P., Grankvist K., Johansson M., Freedman N.D., Huang W.-Y., Chen C., Prentice R., Stevens V.L., Wang Y., Le Marchand L., Wilkens L.R., Weinstein S.J., Albanes D., Cai Q., Blot W.J., Arslan A.A., Zeleniuch-Jacquotte A., Shu X.-O., Zheng W., Yuan J.-M., Koh W.-P., Visvanathan K., Sesso H.D., Zhang X., Gaziano J.M., Fanidi A., Muller D., Brennan P., Guida F., and Robbins H.A.
- Abstract
Imbalances of blood biomarkers are associated with disease, and biomarkers may also vary non-pathologically across population groups. We described variation in concentrations of biomarkers of one-carbon metabolism, vitamin status, inflammation including tryptophan metabolism, and endothelial and renal function among cancer-free older adults. We analyzed 5167 cancer-free controls aged 40-80 years from 20 cohorts in the Lung Cancer Cohort Consortium (LC3). Centralized biochemical analyses of 40 biomarkers in plasma or serum were performed. We fit multivariable linear mixed effects models to quantify variation in standardized biomarker log-concentrations across four factors: age, sex, smoking status, and body mass index (BMI). Differences in most biomarkers across most factors were small, with 93% (186/200) of analyses showing an estimated difference lower than 0.25 standard-deviations, although most were statistically significant due to large sample size. The largest difference was for creatinine by sex, which was-0.91 standard-deviations lower in women than men (95%CI-0.98;-0.84). The largest difference by age was for total cysteine (0.40 standard-deviation increase per 10-year increase, 95%CI 0.36; 0.43), and by BMI was for C-reactive protein (0.38 standard-deviation increase per 5-kg/m2 increase, 95%CI 0.34; 0.41). For 31 of 40 markers, the mean difference between current and never smokers was larger than between former and never smokers. A statistically significant (p<0.05) association with time since smoking cessation was observed for 8 markers, including C-reactive protein, kynurenine, choline, and total homocysteine. We conclude that most blood biomarkers show small variations across demographic characteristics. Patterns by smoking status point to normalization of multiple physiological processes after smoking cessation.
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- 2021
223. Body size and weight change over adulthood and risk of breast cancer by menopausal and hormone receptor status: a pooled analysis of 20 prospective cohort studies.
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Sinha R., Rohan T.E., Sawada N., Schouten L.J., Stolzenberg-Solomon R.Z., Teras L.R., Tsugane S., Visvanathan K., Weiderpass E., White K.K., Willett W.C., Wolk A., Zeleniuch-Jacquotte A., Smith-Warner S.A., van den Brandt P.A., Ziegler R.G., Wang M., Hou T., Li R., Adami H.-O., Agnoli C., Bernstein L., Buring J.E., Chen Y., Connor A.E., Eliassen A.H., Genkinger J.M., Gierach G., Giles G.G., Goodman G.G., Hakansson N., Krogh V., Le Marchand L., Lee I.-M., Liao L.M., Martinez M.E., Miller A.B., Milne R.L., Neuhouser M.L., Patel A.V., Prizment A., Robien K., Sinha R., Rohan T.E., Sawada N., Schouten L.J., Stolzenberg-Solomon R.Z., Teras L.R., Tsugane S., Visvanathan K., Weiderpass E., White K.K., Willett W.C., Wolk A., Zeleniuch-Jacquotte A., Smith-Warner S.A., van den Brandt P.A., Ziegler R.G., Wang M., Hou T., Li R., Adami H.-O., Agnoli C., Bernstein L., Buring J.E., Chen Y., Connor A.E., Eliassen A.H., Genkinger J.M., Gierach G., Giles G.G., Goodman G.G., Hakansson N., Krogh V., Le Marchand L., Lee I.-M., Liao L.M., Martinez M.E., Miller A.B., Milne R.L., Neuhouser M.L., Patel A.V., Prizment A., and Robien K.
- Abstract
Associations between anthropometric factors and breast cancer (BC) risk have varied inconsistently by estrogen and/or progesterone receptor (ER/PR) status. Associations between prediagnostic anthropometric factors and risk of premenopausal and postmenopausal BC overall and ER/PR status subtypes were investigated in a pooled analysis of 20 prospective cohorts, including 36,297 BC cases among 1,061,915 women, using multivariable Cox regression analyses, controlling for reproductive factors, diet and other risk factors. We estimated dose-response relationships and tested for nonlinear associations using restricted cubic splines. Height showed positive, linear associations for premenopausal and postmenopausal BC risk (6-7% RR increase per 5 cm increment), with stronger associations for receptor-positive subtypes. Body mass index (BMI) at cohort baseline was strongly inversely associated with premenopausal BC risk, and strongly positively-and nonlinearly-associated with postmenopausal BC (especially among women who never used hormone replacement therapy). This was primarily observed for receptor-positive subtypes. Early adult BMI (at 18-20 years) showed inverse, linear associations for premenopausal and postmenopausal BC risk (21% and 11% RR decrease per 5 kg/m2, respectively) with stronger associations for receptor-negative subtypes. Adult weight gain since 18-20 years was positively associated with postmenopausal BC risk, stronger for receptor-positive subtypes, and among women who were leaner in early adulthood. Women heavier in early adulthood generally had reduced premenopausal BC risk, independent of later weight gain. Positive associations between height, baseline (adult) BMI, adult weight gain and postmenopausal BC risk were substantially stronger for hormone receptor-positive versus negative subtypes. Premenopausal BC risk was positively associated with height, but inversely with baseline BMI and weight gain (mostly in receptor-positive subtypes). Inverse associ
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- 2021
224. Ovarian cancer risk factor associations by primary anatomic site: The ovarian cancer cohort consortium.
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Fortner R.T., Rice M.S., Knutsen S.F., Orlich M.J., Visvanathan K., Patel A.V., Gaudet M.M., Tjonneland A., Kvaskoff M., Kaaks R., Trichopolou A., Pala V., Charlotte Onland-Moret N., Gram I.T., Amiano P., Idahl A., Allen N.E., Weiderpass E., Poynter J.N., Robien K., Giles G.G., Milne R.L., Setiawan V.W., Merritt M.A., Van Den Brandt P.A., Zeleniuch-Jacquotte A., Arslan A.A., O'Brien K.M., Sandler D.P., Wolk A., Hakansson N., Harris H.R., Trabert B., Wentzensen N., Tworoger S.S., Schouten L.J., Fortner R.T., Rice M.S., Knutsen S.F., Orlich M.J., Visvanathan K., Patel A.V., Gaudet M.M., Tjonneland A., Kvaskoff M., Kaaks R., Trichopolou A., Pala V., Charlotte Onland-Moret N., Gram I.T., Amiano P., Idahl A., Allen N.E., Weiderpass E., Poynter J.N., Robien K., Giles G.G., Milne R.L., Setiawan V.W., Merritt M.A., Van Den Brandt P.A., Zeleniuch-Jacquotte A., Arslan A.A., O'Brien K.M., Sandler D.P., Wolk A., Hakansson N., Harris H.R., Trabert B., Wentzensen N., Tworoger S.S., and Schouten L.J.
- Abstract
Background: Epithelial ovarian, fallopian tube, and primary peritoneal cancers have shared developmental pathways. Few studies have prospectively examined heterogeneity in risk factor associations across these three anatomic sites. Method(s): We identified 3,738 ovarian, 337 peritoneal, and 176 fallopian tube incident cancer cases in 891,731 women from 15 prospective cohorts in the Ovarian Cancer Cohort Consortium. Associations between 18 putative risk factors and risk of ovarian, peritoneal, and fallopian tube cancer, overall and for serous and high-grade serous tumors, were evaluated using competing risks Cox proportional hazards regression. Heterogeneity was assessed by likelihood ratio tests. Result(s): Most associations did not vary by tumor site (Phet >= 0.05). Associations between first pregnancy (Phet 1/4 0.04), tubal ligation (Phet 1/4 0.01), and early-adult (age 18-21 years) body mass index (BMI; Phet 1/4 0.02) and risk differed between ovarian and peritoneal cancers. The association between early-adult BMI and risk further differed between peritoneal and fallopian tube cancer (Phet 1/4 0.03). First pregnancy and tubal ligation were inversely associated with ovarian, but not peritoneal, cancer. Higher early-adult BMI was associated with higher risk of peritoneal, but not ovarian or fallopian tube, cancer. Patterns were generally similar when restricted to serous and high-grade serous cases. Conclusion(s): Ovarian, fallopian tube, and primary peritoneal cancers appear to have both shared and distinct etiologic pathways, although most risk factors appear to have similar associations by anatomic site. Impact: Further studies on the mechanisms underlying the differences in risk profiles may provide insights regarding the developmental origins of tumors arising in the peritoneal cavity and inform prevention efforts.Copyright © 2020 American Association for Cancer Research.
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- 2021
225. Mendelian randomization analysis of n-6 polyunsaturated fatty acid levels and pancreatic cancer risk.
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Ghoneim D.H., Zhu J., Zheng W., Long J., Murff H.J., Ye F., Setiawan V.W., Wilkens L.R., Khankari N.K., Haycock P., Antwi S.O., Yang Y., Arslan A.A., Freeman L.E.B., Bracci P.M., Canzian F., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Marchand L.L., Neale R.E., Scelo G., Visvanathan K., White E., Albane D., Amiano P., Andreott G., Babic A., Bamlet W.R., Berndt S.I., Brais L.K., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Rabe K.G., Chanock S.J., Duggal P., Fuchs C.S., Gaziano J.M., Goggins M.G., Hackert T., Hassan M.M., Helzlsouer K.J., Holly E.A., Hoover R.N., Katske V., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Oberg A.L., Porta M., Rothman N., Sesso H.D., Silverman D.T., Ian T., Wactawski-Wende J., Wang X., Wentzensen N., Yu H., Zeleniuch-Jacquotte A., Yu K., Wolpin B.M., Jacobs E.J., Duell E.J., Risch H.A., Petersen G.M., Amundadottir L.T., Kraft P., Klein A.P., Stolzenberg-Solomon R.Z., Shu X.-O., Wu L., Ghoneim D.H., Zhu J., Zheng W., Long J., Murff H.J., Ye F., Setiawan V.W., Wilkens L.R., Khankari N.K., Haycock P., Antwi S.O., Yang Y., Arslan A.A., Freeman L.E.B., Bracci P.M., Canzian F., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Marchand L.L., Neale R.E., Scelo G., Visvanathan K., White E., Albane D., Amiano P., Andreott G., Babic A., Bamlet W.R., Berndt S.I., Brais L.K., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Rabe K.G., Chanock S.J., Duggal P., Fuchs C.S., Gaziano J.M., Goggins M.G., Hackert T., Hassan M.M., Helzlsouer K.J., Holly E.A., Hoover R.N., Katske V., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Oberg A.L., Porta M., Rothman N., Sesso H.D., Silverman D.T., Ian T., Wactawski-Wende J., Wang X., Wentzensen N., Yu H., Zeleniuch-Jacquotte A., Yu K., Wolpin B.M., Jacobs E.J., Duell E.J., Risch H.A., Petersen G.M., Amundadottir L.T., Kraft P., Klein A.P., Stolzenberg-Solomon R.Z., Shu X.-O., and Wu L.
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Background: Whether circulating polyunsaturated fatty acid (PUFA) levels are associated with pancreatic cancer risk is uncertain. Mendelian randomization (MR) represents a study design using genetic instruments to better characterize the relationship between exposure and outcome. Method(s): We utilized data from genome-wide association studies within the Pancreatic Cancer Cohort Consortium and Pancreatic Cancer Case-Control Consortium, involving approximately 9,269 cases and 12,530 controls of European descent, to evaluate associations between pancreatic cancer risk and genetically predicted plasma n-6 PUFA levels. Conventional MR analyses were performed using individual-level and summary-level data. Result(s): Using genetic instruments, we did not find evidence of associations between genetically predicted plasma n-6 PUFA levels and pancreatic cancer risk [estimates per one SD increase in each PUFA-specific weighted genetic score using summary statistics: Linoleic acid odds ratio (OR)1.00, 95% confidence interval (CI) 0.98-1.02; arachidonic acid OR 1.00, 95% CI 0.99-1.01; and dihomo-gamma-linolenic acid OR 0.95, 95% CI 0.87-1.02]. The OR estimates remained virtually unchanged after adjustment for covariates, using individual-level data or summary statistics, or stratification by age and sex. Conclusion(s): Our results suggest that variations of genetically determined plasma n-6 PUFA levels are not associated with pancreatic cancer risk. Impact: These results suggest that modifying n-6 PUFA levels through food sources or supplementation may not influence risk of pancreatic cancer.Copyright © 2020 American Association for Cancer Research Inc.. All rights reserved.
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- 2021
226. Cohort Profile: The Ovarian Cancer Cohort Consortium (OC3).
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Townsend M.K., Trabert B., Fortner R.T., Arslan A.A., Buring J.E., Carter B.D., Giles G.G., Irvin S.R., Jones M.E., Kaaks R., Kirsh V.A., Knutsen S.F., Koh W.-P., Lacey J.V., Langseth H., Larsson S.C., Lee I.-M., Martinez M.E., Merritt M.A., Milne R.L., O'Brien K.M., Orlich M.J., Palmer J.R., Patel A.V., Peters U., Poynter J.N., Robien K., Rohan T.E., Rosenberg L., Sandin S., Sandler D.P., Schouten L.J., Setiawan V.W., Swerdlow A.J., Ursin G., van den Brandt P.A., Visvanathan K., Weiderpass E., Wolk A., Yuan J.-M., Zeleniuch-Jacquotte A., Tworoger S.S., Wentzensen N., Townsend M.K., Trabert B., Fortner R.T., Arslan A.A., Buring J.E., Carter B.D., Giles G.G., Irvin S.R., Jones M.E., Kaaks R., Kirsh V.A., Knutsen S.F., Koh W.-P., Lacey J.V., Langseth H., Larsson S.C., Lee I.-M., Martinez M.E., Merritt M.A., Milne R.L., O'Brien K.M., Orlich M.J., Palmer J.R., Patel A.V., Peters U., Poynter J.N., Robien K., Rohan T.E., Rosenberg L., Sandin S., Sandler D.P., Schouten L.J., Setiawan V.W., Swerdlow A.J., Ursin G., van den Brandt P.A., Visvanathan K., Weiderpass E., Wolk A., Yuan J.-M., Zeleniuch-Jacquotte A., Tworoger S.S., and Wentzensen N.
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- 2021
227. Dairy foods, calcium, and risk of breast cancer overall and for subtypes defined by estrogen receptor status: a pooled analysis of 21 cohort studies.
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Wu Y., Huang R., Wang M., Bernstein L., Bethea T.N., Chen C., Chen Y., Eliassen A.H., Freedman N.D., Gaudet M.M., Gierach G.L., Giles G.G., Krogh V., Larsson S.C., Liao L.M., Mccullough M.L., Miller A.B., Milne R.L., Monroe K.R., Neuhouser M.L., Palmer J.R., Prizment A., Reynolds P., Robien K., Rohan T.E., Sandin S., Sawada N., Sieri S., Sinha R., Stolzenberg-Solomon R.Z., Tsugane S., Van Den Brandt P.A., Visvanathan K., Weiderpass E., Wilkens L.R., Willett W.C., Wolk A., Zeleniuch-Jacquotte A., Ziegler R.G., Smith-Warner S.A., Wu Y., Huang R., Wang M., Bernstein L., Bethea T.N., Chen C., Chen Y., Eliassen A.H., Freedman N.D., Gaudet M.M., Gierach G.L., Giles G.G., Krogh V., Larsson S.C., Liao L.M., Mccullough M.L., Miller A.B., Milne R.L., Monroe K.R., Neuhouser M.L., Palmer J.R., Prizment A., Reynolds P., Robien K., Rohan T.E., Sandin S., Sawada N., Sieri S., Sinha R., Stolzenberg-Solomon R.Z., Tsugane S., Van Den Brandt P.A., Visvanathan K., Weiderpass E., Wilkens L.R., Willett W.C., Wolk A., Zeleniuch-Jacquotte A., Ziegler R.G., and Smith-Warner S.A.
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Background: Epidemiologic studies examining the relations between dairy product and calcium intakes and breast cancer have been inconclusive, especially for tumor subtypes. Objective(s): To evaluate the associations between intakes of specific dairy products and calcium and risk of breast cancer overall and for subtypes defined by estrogen receptor (ER) status. Method(s): We pooled the individual-level data of over 1 million women who were followed for a maximum of 8-20 years across studies. Associations were evaluated for dairy product and calcium intakes and risk of incident invasive breast cancer overall (n = 37,861 cases) and by subtypes defined by ER status. Study-specific multivariable hazard ratios (HRs) were estimated and then combined using random-effects models. Result(s): Overall, no clear association was observed between the consumption of specific dairy foods, dietary (from foods only) calcium, and total (from foods and supplements) calcium, and risk of overall breast cancer. Although each dairy product showed a null or very weak inverse association with risk of overall breast cancer (P, test for trend >0.05 for all), differences by ER status were suggested for yogurt and cottage/ricotta cheese with associations observed for ER-negative tumors only (pooled HR = 0.90, 95% CI: 0.83, 0.98 comparing >=60 g/d with <1 g/d of yogurt and 0.85, 95% CI: 0.76, 0.95 comparing >=25 g/d with <1 g/d of cottage/ricotta cheese). Dietary calcium intake was only weakly associated with breast cancer risk (pooled HR = 0.98, 95% CI: 0.97, 0.99 per 350 mg/d). Conclusion(s): Our study shows that adult dairy or calcium consumption is unlikely to associate with a higher risk of breast cancer and that higher yogurt and cottage/ricotta cheese intakes were inversely associated with the risk of ER-negative breast cancer, a less hormonally dependent subtype with poor prognosis. Future studies on fermented dairy products, earlier life exposures, ER-negative breast cancer, and differen
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- 2021
228. Genome-wide genediabetes and geneobesity interaction scan in 8,255 cases and 11,900 controls from panscan and PanC4 consortia.
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Campa D., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Blackford A., Bueno-De-Mesquita B., Buring J.E., Chanock S.J., Childs E., Duell E.J., Fuchs C., Michael Gaziano J., Goggins M., Hartge P., Hassam M.H., Holly E.A., Hoover R.N., Hung R.J., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Ng K., Oberg A.L., Orlow I., Peters U., Porta M., Rabe K.G., Rothman N., Scelo G., Sesso H.D., Silverman D.T., Thompson I.M., Tjonneland A., Trichopoulou A., Wactawski-Wende J., Wentzensen N., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Amundadottir L.T., Jacobs E.J., Petersen G.M., Wolpin B.M., Risch H.A., Chatterjee N., Klein A.P., Li D., Kraft P., Wei P., Tang H., Jiang L., Stolzenberg-Solomon R.Z., Arslan A.A., Beane Freeman L.E., Bracci P.M., Brennan P., Canzian F., Du M., Gallinger S., Giles G.G., Campa D., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Blackford A., Bueno-De-Mesquita B., Buring J.E., Chanock S.J., Childs E., Duell E.J., Fuchs C., Michael Gaziano J., Goggins M., Hartge P., Hassam M.H., Holly E.A., Hoover R.N., Hung R.J., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Ng K., Oberg A.L., Orlow I., Peters U., Porta M., Rabe K.G., Rothman N., Scelo G., Sesso H.D., Silverman D.T., Thompson I.M., Tjonneland A., Trichopoulou A., Wactawski-Wende J., Wentzensen N., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Amundadottir L.T., Jacobs E.J., Petersen G.M., Wolpin B.M., Risch H.A., Chatterjee N., Klein A.P., Li D., Kraft P., Wei P., Tang H., Jiang L., Stolzenberg-Solomon R.Z., Arslan A.A., Beane Freeman L.E., Bracci P.M., Brennan P., Canzian F., Du M., Gallinger S., and Giles G.G.
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Background: Obesity and diabetes are major modifiable risk factors for pancreatic cancer. Interactions between genetic variants and diabetes/obesity have not previously been comprehensively investigated in pancreatic cancer at the genome-wide level. Method(s): We conducted a gene-environment interaction (GxE) analysis including 8,255 cases and 11,900 controls from four pancreatic cancer genome-wide association study (GWAS) datasets (Pancreatic Cancer Cohort Consortium I-III and Pancreatic Cancer Case Control Consortium). Obesity (body mass index >=30 kg/m2) and diabetes (duration >=3 years) were the environmental variables of interest. Approximately 870,000 SNPs (minor allele frequency >=0.005, genotyped in at least one dataset) were analyzed. Case-control (CC), case-only (CO), and joint-effect test methods were used for SNP-level GxE analysis. As a complementary approach, gene-based GxE analysis was also performed. Age, sex, study site, and principal components accounting for population substructure were included as covariates. Meta-analysis was applied to combine individual GWAS summary statistics. Result(s): No genome-wide significant interactions (departures from a log-additive odds model) with diabetes or obesity were detected at the SNP level by the CC or CO approaches. The joint-effect test detected numerous genome-wide significant GxE signals in the GWAS main effects top hit regions, but the significance diminished after adjusting for the GWAS top hits. In the gene-based analysis, a significant interaction of diabetes with variants in the FAM63A (family with sequence similarity 63 member A) gene (significance threshold P < 1.25 106) was observed in the meta-analysis (PGxE 1/4 1.2 106, PJoint 1/4 4.2 107). Conclusion(s): This analysis did not find significant GxE interactions at the SNP level but found one significant interaction with diabetes at the gene level. A larger sample size might unveil additional genetic factors via GxE scans. Impact: This study may
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- 2021
229. Smoking modifies pancreatic cancer risk loci on 2q21.3.
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Mocci E., Kundu P., Wheeler W., Arslan A.A., Beane-Freeman L.E., Bracci P.M., Brennan P., Canzian F., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Blackford A.L., Bueno-De-Mesquita B., Buring J.E., Campa D., Chanock S.J., Childs E.J., Duell E.J., Fuchs C.S., Gaziano J.M., Giovannucci E.L., Goggins M.G., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Hung R.J., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Ng K., Oberg A.L., Panico S., Peters U., Porta M., Rabe K.G., Riboli E., Rothman N., Scelo G., Sesso H.D., Silverman D.T., Stevens V.L., Strobel O., Thompson I.M., Tjonneland A., Trichopoulou A., van Den Eeden S.K., Wactawski-Wende J., Wentzensen N., Wilkens L.R., Yu H., Yuan F., Zeleniuch-Jacquotte A., Amundadottir L.T., Li D., Jacobs E.J., Petersen G.M., Wolpin B.M., Risch H.A., Kraft P., Chatterjee N., Klein A.P., Stolzenberg-Solomon R., Mocci E., Kundu P., Wheeler W., Arslan A.A., Beane-Freeman L.E., Bracci P.M., Brennan P., Canzian F., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Blackford A.L., Bueno-De-Mesquita B., Buring J.E., Campa D., Chanock S.J., Childs E.J., Duell E.J., Fuchs C.S., Gaziano J.M., Giovannucci E.L., Goggins M.G., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Hung R.J., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Ng K., Oberg A.L., Panico S., Peters U., Porta M., Rabe K.G., Riboli E., Rothman N., Scelo G., Sesso H.D., Silverman D.T., Stevens V.L., Strobel O., Thompson I.M., Tjonneland A., Trichopoulou A., van Den Eeden S.K., Wactawski-Wende J., Wentzensen N., Wilkens L.R., Yu H., Yuan F., Zeleniuch-Jacquotte A., Amundadottir L.T., Li D., Jacobs E.J., Petersen G.M., Wolpin B.M., Risch H.A., Kraft P., Chatterjee N., Klein A.P., and Stolzenberg-Solomon R.
- Abstract
Germline variation and smoking are independently associated with pancreatic ductal adenocarcinoma (PDAC). We conducted genome-wide smoking interaction analysis of PDAC using genotype data from four previous genome-wide association studies in individuals of European ancestry (7,937 cases and 11,774 controls). Examination of expression quantitative trait loci data from the Genotype-Tissue Expression Project followed by colocalization analysis was conducted to determine whether there was support for common SNP(s) underlying the observed associations. Statistical tests were two sided and P < 5 10-8 was considered statistically significant. Genome-wide significant evidence of qualitative interaction was identified on chr2q21.3 in intron 5 of the transmembrane protein 163 (TMEM163) and upstream of the cyclin T2 (CCNT2). The most significant SNP using the Empirical Bayes method, in this region that included 45 significantly associated SNPs, was rs1818613 [per allele OR in never smokers 0.87, 95% confidence interval (CI), 0.82-0.93; former smokers 1.00, 95% CI, 0.91-1.07; current smokers 1.25, 95% CI 1.12-1.40, Pinteraction 1/4 3.08 10-9). Examination of the Genotype-Tissue Expression Project data demonstrated an expression quantitative trait locus in this region for TMEM163 and CCNT2 in several tissue types. Colocalization analysis supported a shared SNP, rs842357, in high linkage disequilibrium with rs1818613 (r2 1/4 0. 94) driving both the observed interaction and the expression quantitative trait loci signals. Future studies are needed to confirm and understand the differential biologic mechanisms by smoking status that contribute to our PDAC findings.Copyright © 2021 American Association for Cancer Research.
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- 2021
230. Hepcidin-regulating iron metabolism genes and pancreatic ductal adenocarcinoma: a pathway analysis of genome-wide association studies.
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Julian-Serrano S., Yuan F., Wheeler W., Benyamin B., Machiela M.J., Arslan A.A., Beane-Freeman L.E., Bracci P.M., Duell E.J., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Marchand L.L., Neale R.E., Shu X.-O., Van Den Eeden S.K., Visvanathan K., Zheng W., Albanes D., Andreotti G., Ardanaz E., Babic A., Berndt S.I., Brais L.K., Brennan P., Bueno-de-Mesquita B., Buring J.E., Chanock S.J., Childs E.J., Chung C.C., Fabianova E., Foretova L., Fuchs C.S., Gaziano J.M., Gentiluomo M., Giovannucci E.L., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holcatova I., Holly E.A., Hung R.I., Janout V., Kurtz R.C., Lee I.-M., Malats N., McKean D., Milne R.L., Newton C.C., Oberg A.L., Perdomo S., Peters U., Porta M., Rothman N., Schulze M.B., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., Weiderpass E., Wenstzensen N., White E., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Zhong J., Kraft P., Li D., Campbell P.T., Petersen G.M., Wolpin B.M., Risch H.A., Amundadottir L.T., Klein A.P., Yu K., Stolzenberg-Solomon R.Z., Julian-Serrano S., Yuan F., Wheeler W., Benyamin B., Machiela M.J., Arslan A.A., Beane-Freeman L.E., Bracci P.M., Duell E.J., Du M., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Marchand L.L., Neale R.E., Shu X.-O., Van Den Eeden S.K., Visvanathan K., Zheng W., Albanes D., Andreotti G., Ardanaz E., Babic A., Berndt S.I., Brais L.K., Brennan P., Bueno-de-Mesquita B., Buring J.E., Chanock S.J., Childs E.J., Chung C.C., Fabianova E., Foretova L., Fuchs C.S., Gaziano J.M., Gentiluomo M., Giovannucci E.L., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holcatova I., Holly E.A., Hung R.I., Janout V., Kurtz R.C., Lee I.-M., Malats N., McKean D., Milne R.L., Newton C.C., Oberg A.L., Perdomo S., Peters U., Porta M., Rothman N., Schulze M.B., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., Weiderpass E., Wenstzensen N., White E., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Zhong J., Kraft P., Li D., Campbell P.T., Petersen G.M., Wolpin B.M., Risch H.A., Amundadottir L.T., Klein A.P., Yu K., and Stolzenberg-Solomon R.Z.
- Abstract
BACKGROUND: Epidemiological studies have suggested positive associations for iron and red meat intake with risk of pancreatic ductal adenocarcinoma (PDAC). Inherited pathogenic variants in genes involved in the hepcidin-regulating iron metabolism pathway are known to cause iron overload and hemochromatosis. OBJECTIVE(S): The objective of this study was to determine whether common genetic variation in the hepcidin-regulating iron metabolism pathway is associated with PDAC. METHOD(S): We conducted a pathway analysis of the hepcidin-regulating genes using single nucleotide polymorphism (SNP) summary statistics generated from 4 genome-wide association studies in 2 large consortium studies using the summary data-based adaptive rank truncated product method. Our population consisted of 9253 PDAC cases and 12,525 controls of European descent. Our analysis included 11 hepcidin-regulating genes [bone morphogenetic protein 2 (BMP2), bone morphogenetic protein 6 (BMP6), ferritin heavy chain 1 (FTH1), ferritin light chain (FTL), hepcidin (HAMP), homeostatic iron regulator (HFE), hemojuvelin (HJV), nuclear factor erythroid 2-related factor 2 (NRF2), ferroportin 1 (SLC40A1), transferrin receptor 1 (TFR1), and transferrin receptor 2 (TFR2)] and their surrounding genomic regions (+/-20 kb) for a total of 412 SNPs. RESULT(S): The hepcidin-regulating gene pathway was significantly associated with PDAC (P = 0.002), with the HJV, TFR2, TFR1, BMP6, and HAMP genes contributing the most to the association. CONCLUSION(S): Our results support that genetic susceptibility related to the hepcidin-regulating gene pathway is associated with PDAC risk and suggest a potential role of iron metabolism in pancreatic carcinogenesis. Further studies are needed to evaluate effect modification by intake of iron-rich foods on this association.Copyright Published by Oxford University Press on behalf of the American Society for Nutrition 2021.
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- 2021
231. Genome-wide association study data reveal genetic susceptibility to chronic inflammatory intestinal diseases and pancreatic ductal adenocarcinoma risk.
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Wang X., Yuan F., Hung R.J., Walsh N., Zhang H., Platz E.A., Wheeler W., Song L., Arslan A.A., Beane Freeman L.E., Bracci P., Canzian F., Du M., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Shi J., Duell E.J., Amundadottir L.T., Li D., Petersen G.M., Wolpin B.M., Risch H.A., Yu K., Klein A.P., Stolzenberg-Solomon R., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Rosendahl J., Scelo G., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Amiano P., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Chanock S.J., Fuchs C.S., Michael Gaziano J., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Katzke V., Kirsten H., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Ng K., Oberg A.L., Porta M., Rabe K.G., Real F.X., Rothman N., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., Wentzensen N., Wang X., Yuan F., Hung R.J., Walsh N., Zhang H., Platz E.A., Wheeler W., Song L., Arslan A.A., Beane Freeman L.E., Bracci P., Canzian F., Du M., Wilkens L.R., Yu H., Zeleniuch-Jacquotte A., Shi J., Duell E.J., Amundadottir L.T., Li D., Petersen G.M., Wolpin B.M., Risch H.A., Yu K., Klein A.P., Stolzenberg-Solomon R., Gallinger S., Giles G.G., Goodman P.J., Kooperberg C., Le Marchand L., Neale R.E., Rosendahl J., Scelo G., Shu X.-O., Visvanathan K., White E., Zheng W., Albanes D., Amiano P., Andreotti G., Babic A., Bamlet W.R., Berndt S.I., Brennan P., Bueno-De-Mesquita B., Buring J.E., Campbell P.T., Chanock S.J., Fuchs C.S., Michael Gaziano J., Goggins M.G., Hackert T., Hartge P., Hassan M.M., Holly E.A., Hoover R.N., Katzke V., Kirsten H., Kurtz R.C., Lee I.-M., Malats N., Milne R.L., Murphy N., Ng K., Oberg A.L., Porta M., Rabe K.G., Real F.X., Rothman N., Sesso H.D., Silverman D.T., Thompson I.M., Wactawski-Wende J., and Wentzensen N.
- Abstract
Registry-based epidemiologic studies suggest associations between chronic inflammatory intestinal diseases and pancreatic ductal adenocarcinoma (PDAC). As genetic susceptibility contributes to a large proportion of chronic inflammatory intestinal diseases, we hypothesize that the genomic regions surrounding established genome-wide associated variants for these chronic inflammatory diseases are associated with PDAC. We examined the association between PDAC and genomic regions (+500 kb) surrounding established common susceptibility variants for ulcerative colitis, Crohn's disease, inflammatory bowel disease, celiac disease, chronic pancreatitis, and primary sclerosing cholangitis. We analyzed summary statistics from genome-wide association studies data for 8,384 cases and 11,955 controls of European descent from two large consortium studies using the summary data-based adaptive rank truncated product method to examine the overall association of combined genomic regions for each inflammatory disease group. Combined genomic susceptibility regions for ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis were associated with PDAC at P values < 0.05 (0.0040, 0.0057, 0.011, and 3.4 x 10-6, respectively). After excluding the 20 PDAC susceptibility regions (+500 kb) previously identified by GWAS, the genomic regions for ulcerative colitis, Crohn disease, and inflammatory bowel disease remained associated with PDAC (P 1/4 0.0029, 0.0057, and 0.0098, respectively). Genomic regions for celiac disease (P 1/4 0.22) and primary sclerosing cholangitis (P 1/4 0.078) were not associated with PDAC. Our results support the hypothesis that genomic regions surrounding variants associated with inflammatory intestinal diseases, particularly, ulcerative colitis, Crohn disease, inflammatory bowel disease, and chronic pancreatitis are associated with PDAC.Copyright © 2020 American Association for Cancer Research.
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- 2021
232. A transcriptome-wide association study identifies novel candidate susceptibility genes for pancreatic cancer.
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Hasan M., Zhang T., Xiao W., Albanes D., Andreotti G., Arslan A.A., Babic A., Bamlet W.R., Beane-Freeman L., Berndt S., Borgida A., Bracci P.M., Brais L., Brennan P., Bueno-De-Mesquita B., Buring J., Canzian F., Childs E.J., Cotterchio M., Du M., Duell E.J., Fuchs C., Gallinger S., Michael Gaziano J., Giles G.G., Giovannucci E., Goggins M., Goodman G.E., Goodman P.J., Haiman C., Hartge P., Helzlsouer K.J., Holly E.A., Klein E.A., Kogevinas M., Kurtz R.J., LeMarchand L., Malats N., Mannisto S., Milne R., Neale R.E., Ng K., Obazee O., Oberg A.L., Orlow I., Patel A.V., Peters U., Porta M., Rothman N., Scelo G., Sesso H.D., Severi G., Sieri S., Silverman D., Sund M., Tjonneland A., Thornquist M.D., Tobias G.S., Trichopoulou A., van Den Eeden S.K., Visvanathan K., Wactawski-Wende J., Wentzensen N., White E., Yu H., Yuan C., Zeleniuch-Jacquotte A., Hoover R., Brown K., Kooperberg C., Risch H.A., Jacobs E.J., Li D., Yu K., Shu X.-O., Chanock S.J., Wolpin B.M., Stolzenberg-Solomon R.Z., Chatterjee N., Klein A.P., Smith J.P., Kraft P., Shi J., Petersen G.M., Zheng W., Amundadottir L.T., Zhong J., Jermusyk A., Wu L., Hoskins J.W., Collins I., Mocci E., Zhang M., Song L., Chung C.C., Hasan M., Zhang T., Xiao W., Albanes D., Andreotti G., Arslan A.A., Babic A., Bamlet W.R., Beane-Freeman L., Berndt S., Borgida A., Bracci P.M., Brais L., Brennan P., Bueno-De-Mesquita B., Buring J., Canzian F., Childs E.J., Cotterchio M., Du M., Duell E.J., Fuchs C., Gallinger S., Michael Gaziano J., Giles G.G., Giovannucci E., Goggins M., Goodman G.E., Goodman P.J., Haiman C., Hartge P., Helzlsouer K.J., Holly E.A., Klein E.A., Kogevinas M., Kurtz R.J., LeMarchand L., Malats N., Mannisto S., Milne R., Neale R.E., Ng K., Obazee O., Oberg A.L., Orlow I., Patel A.V., Peters U., Porta M., Rothman N., Scelo G., Sesso H.D., Severi G., Sieri S., Silverman D., Sund M., Tjonneland A., Thornquist M.D., Tobias G.S., Trichopoulou A., van Den Eeden S.K., Visvanathan K., Wactawski-Wende J., Wentzensen N., White E., Yu H., Yuan C., Zeleniuch-Jacquotte A., Hoover R., Brown K., Kooperberg C., Risch H.A., Jacobs E.J., Li D., Yu K., Shu X.-O., Chanock S.J., Wolpin B.M., Stolzenberg-Solomon R.Z., Chatterjee N., Klein A.P., Smith J.P., Kraft P., Shi J., Petersen G.M., Zheng W., Amundadottir L.T., Zhong J., Jermusyk A., Wu L., Hoskins J.W., Collins I., Mocci E., Zhang M., Song L., and Chung C.C.
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Background: Although 20 pancreatic cancer susceptibility loci have been identified through genome-wide association studies in individuals of European ancestry, much of its heritability remains unexplained and the genes responsible largely unknown. Method(s): To discover novel pancreatic cancer risk loci and possible causal genes, we performed a pancreatic cancer transcriptome-wide association study in Europeans using three approaches: FUSION, MetaXcan, and Summary-MulTiXcan. We integrated genome-wide association studies summary statistics from 9040 pancreatic cancer cases and 12 496 controls, with gene expression prediction models built using transcriptome data from histologically normal pancreatic tissue samples (NCI Laboratory of Translational Genomics [n = 95] and Genotype-Tissue Expression v7 [n = 174] datasets) and data from 48 different tissues (Genotype-Tissue Expression v7, n = 74-421 samples). Result(s): We identified 25 genes whose genetically predicted expression was statistically significantly associated with pancreatic cancer risk (false discovery rate <.05), including 14 candidate genes at 11 novel loci (1p36.12: CELA3B; 9q31.1: SMC2, SMC2-AS1; 10q23.31: RP11-80H5.9; 12q13.13: SMUG1; 14q32.33: BTBD6; 15q23: HEXA; 15q26.1: RCCD1; 17q12: PNMT, CDK12, PGAP3; 17q22: SUPT4H1; 18q11.22:RP11-888D10.3; and 19p13.11: PGPEP1) and 11 at six known risk loci (5p15.33: TERT, CLPTM1L, ZDHHC11B; 7p14.1: INHBA; 9q34.2: ABO; 13q12.2: PDX1; 13q22.1: KLF5; and 16q23.1: WDR59, CFDP1, BCAR1, TMEM170A). The association for 12 of these genes (CELA3B, SMC2, and PNMT at novel risk loci and TERT, CLPTM1L, INHBA, ABO, PDX1, KLF5, WDR59, CFDP1, and BCAR1 at known loci) remained statistically significant after Bonferroni correction. Conclusion(s): By integrating gene expression and genotype data, we identified novel pancreatic cancer risk loci and candidate functional genes that warrant further investigation.Copyright © 2020 Oxford University Press. All rights reserved.
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- 2021
233. Pregnancy outcomes and risk of endometrial cancer: A pooled analysis of individual participant data in the Epidemiology of Endometrial Cancer Consortium
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Jordan, Susan J., Jordan, Susan J., Na, Renhua, Weiderpass, Elisabete, Adami, Hans-Olov, Anderson, Kristin E., van den Brandt, Piet A., Brinton, Louise A., Chen, Chu, Cook, Linda S., Doherty, Jennifer A., Du, Mengmeng, Friedenreich, Christine M., Gierach, Gretchen L., Goodman, Marc T., Krogh, Vittorio, Levi, Fabio, Lu, Lingeng, Miller, Anthony B., McCann, Susan E., Moysich, Kirsten B., Negri, Eva, Olson, Sara H., Petruzella, Stacey, Palmer, Julie R., Parazzini, Fabio, Pike, Malcolm C., Prizment, Anna E., Rebbeck, Timothy R., Reynolds, Peggy, Ricceri, Fulvio, Risch, Harvey A., Rohan, Thomas E., Sacerdote, Carlotta, Schouten, Leo J., Serraino, Diego, Setiawan, Veronica W., Shu, Xiao-Ou, Sponholtz, Todd R., Spurdle, Amanda B., Stolzenberg-Solomon, Rachael Z., Trabert, Britton, Wentzensen, Nicolas, Wilkens, Lynne R., Wise, Lauren A., Yu, Herbert, La Vecchia, Carlo, De Vivo, Immaculata, Xu, Wanghong, Zeleniuch-Jacquotte, Anne, Webb, Penelope M., Jordan, Susan J., Jordan, Susan J., Na, Renhua, Weiderpass, Elisabete, Adami, Hans-Olov, Anderson, Kristin E., van den Brandt, Piet A., Brinton, Louise A., Chen, Chu, Cook, Linda S., Doherty, Jennifer A., Du, Mengmeng, Friedenreich, Christine M., Gierach, Gretchen L., Goodman, Marc T., Krogh, Vittorio, Levi, Fabio, Lu, Lingeng, Miller, Anthony B., McCann, Susan E., Moysich, Kirsten B., Negri, Eva, Olson, Sara H., Petruzella, Stacey, Palmer, Julie R., Parazzini, Fabio, Pike, Malcolm C., Prizment, Anna E., Rebbeck, Timothy R., Reynolds, Peggy, Ricceri, Fulvio, Risch, Harvey A., Rohan, Thomas E., Sacerdote, Carlotta, Schouten, Leo J., Serraino, Diego, Setiawan, Veronica W., Shu, Xiao-Ou, Sponholtz, Todd R., Spurdle, Amanda B., Stolzenberg-Solomon, Rachael Z., Trabert, Britton, Wentzensen, Nicolas, Wilkens, Lynne R., Wise, Lauren A., Yu, Herbert, La Vecchia, Carlo, De Vivo, Immaculata, Xu, Wanghong, Zeleniuch-Jacquotte, Anne, and Webb, Penelope M.
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A full-term pregnancy is associated with reduced endometrial cancer risk; however, whether the effect of additional pregnancies is independent of age at last pregnancy is unknown. The associations between other pregnancy-related factors and endometrial cancer risk are less clear. We pooled individual participant data from 11 cohort and 19 case-control studies participating in the Epidemiology of Endometrial Cancer Consortium (E2C2) including 16 986 women with endometrial cancer and 39 538 control women. We used one- and two-stage meta-analytic approaches to estimate pooled odds ratios (ORs) for the association between exposures and endometrial cancer risk. Ever having a full-term pregnancy was associated with a 41% reduction in risk of endometrial cancer compared to never having a full-term pregnancy (OR = 0.59, 95% confidence interval [CI] 0.56-0.63). The risk reduction appeared the greatest for the first full-term pregnancy (OR = 0.78, 95% CI 0.72-0.84), with a further similar to 15% reduction per pregnancy up to eight pregnancies (OR = 0.20, 95% CI 0.14-0.28) that was independent of age at last full-term pregnancy. Incomplete pregnancy was also associated with decreased endometrial cancer risk (7%-9% reduction per pregnancy). Twin births appeared to have the same effect as singleton pregnancies. Our pooled analysis shows that, while the magnitude of the risk reduction is greater for a full-term pregnancy than an incomplete pregnancy, each additional pregnancy is associated with further reduction in endometrial cancer risk, independent of age at last full-term pregnancy. These results suggest that the very high progesterone level in the last trimester of pregnancy is not the sole explanation for the protective effect of pregnancy.
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- 2021
234. Smoking Modifies Pancreatic Cancer Risk Loci on 2q21.3
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Mocci, E, Kundu, P, Wheeler, W, Arslan, AA, Beane-Freeman, LE, Bracci, PM, Brennan, P, Canzian, F, Du, M, Gallinger, S, Giles, GG, Goodman, PJ, Kooperberg, C, Le Marchand, L, Neale, RE, Shu, X-O, Visvanathan, K, White, E, Zheng, W, Albanes, D, Andreotti, G, Babic, A, Bamlet, WR, Berndt, S, Blackford, AL, Bueno-de-Mesquita, B, Buring, JE, Campa, D, Chanock, SJ, Childs, EJ, Duell, EJ, Fuchs, CS, Gaziano, JM, Giovannucci, EL, Goggins, MG, Hartge, P, Hassan, MM, Holly, EA, Hoover, RN, Hung, RJ, Kurtz, RC, Lee, I-M, Malats, N, Milne, RL, Ng, K, Oberg, AL, Panico, S, Peters, U, Porta, M, Rabe, KG, Riboli, E, Rothman, N, Scelo, G, Sesso, HD, Silverman, DT, Stevens, VL, Strobel, O, Thompson, IM, Tjonneland, A, Trichopoulou, A, Van den Eeden, SK, Wactawski-Wende, J, Wentzensen, N, Wilkens, LR, Yu, H, Yuan, F, Zeleniuch-Jacquotte, A, Amundadottir, LT, Li, D, Jacobs, EJ, Petersen, GM, Wolpin, BM, Risch, HA, Kraft, P, Chatterjee, N, Klein, AP, Stolzenberg-Solomon, R, Mocci, E, Kundu, P, Wheeler, W, Arslan, AA, Beane-Freeman, LE, Bracci, PM, Brennan, P, Canzian, F, Du, M, Gallinger, S, Giles, GG, Goodman, PJ, Kooperberg, C, Le Marchand, L, Neale, RE, Shu, X-O, Visvanathan, K, White, E, Zheng, W, Albanes, D, Andreotti, G, Babic, A, Bamlet, WR, Berndt, S, Blackford, AL, Bueno-de-Mesquita, B, Buring, JE, Campa, D, Chanock, SJ, Childs, EJ, Duell, EJ, Fuchs, CS, Gaziano, JM, Giovannucci, EL, Goggins, MG, Hartge, P, Hassan, MM, Holly, EA, Hoover, RN, Hung, RJ, Kurtz, RC, Lee, I-M, Malats, N, Milne, RL, Ng, K, Oberg, AL, Panico, S, Peters, U, Porta, M, Rabe, KG, Riboli, E, Rothman, N, Scelo, G, Sesso, HD, Silverman, DT, Stevens, VL, Strobel, O, Thompson, IM, Tjonneland, A, Trichopoulou, A, Van den Eeden, SK, Wactawski-Wende, J, Wentzensen, N, Wilkens, LR, Yu, H, Yuan, F, Zeleniuch-Jacquotte, A, Amundadottir, LT, Li, D, Jacobs, EJ, Petersen, GM, Wolpin, BM, Risch, HA, Kraft, P, Chatterjee, N, Klein, AP, and Stolzenberg-Solomon, R
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Germline variation and smoking are independently associated with pancreatic ductal adenocarcinoma (PDAC). We conducted genome-wide smoking interaction analysis of PDAC using genotype data from four previous genome-wide association studies in individuals of European ancestry (7,937 cases and 11,774 controls). Examination of expression quantitative trait loci data from the Genotype-Tissue Expression Project followed by colocalization analysis was conducted to determine whether there was support for common SNP(s) underlying the observed associations. Statistical tests were two sided and P < 5 × 10-8 was considered statistically significant. Genome-wide significant evidence of qualitative interaction was identified on chr2q21.3 in intron 5 of the transmembrane protein 163 (TMEM163) and upstream of the cyclin T2 (CCNT2). The most significant SNP using the Empirical Bayes method, in this region that included 45 significantly associated SNPs, was rs1818613 [per allele OR in never smokers 0.87, 95% confidence interval (CI), 0.82-0.93; former smokers 1.00, 95% CI, 0.91-1.07; current smokers 1.25, 95% CI 1.12-1.40, P interaction = 3.08 × 10-9). Examination of the Genotype-Tissue Expression Project data demonstrated an expression quantitative trait locus in this region for TMEM163 and CCNT2 in several tissue types. Colocalization analysis supported a shared SNP, rs842357, in high linkage disequilibrium with rs1818613 (r 2 = 0. 94) driving both the observed interaction and the expression quantitative trait loci signals. Future studies are needed to confirm and understand the differential biologic mechanisms by smoking status that contribute to our PDAC findings. SIGNIFICANCE: This large genome-wide interaction study identifies a susceptibility locus on 2q21.3 that significantly modified PDAC risk by smoking status, providing insight into smoking-associated PDAC, with implications for prevention.
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- 2021
235. Epidemiology of 40 blood biomarkers of one-carbon metabolism, vitamin status, inflammation, and renal and endothelial function among cancer-free older adults
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Zahed, H, Johansson, M, Ueland, PM, Midttun, O, Milne, RL, Giles, GG, Manjer, J, Sandsveden, M, Langhammer, A, Sorgjerd, EP, Grankvist, K, Freedman, ND, Huang, W-Y, Chen, C, Prentice, R, Stevens, VL, Wang, Y, Le Marchand, L, Wilkens, LR, Weinstein, SJ, Albanes, D, Cai, Q, Blot, WJ, Arslan, AA, Zeleniuch-Jacquotte, A, Shu, X-O, Zheng, W, Yuan, J-M, Koh, W-P, Visvanathan, K, Sesso, HD, Zhang, X, Gaziano, JM, Fanidi, A, Muller, D, Brennan, P, Guida, F, Robbins, HA, Zahed, H, Johansson, M, Ueland, PM, Midttun, O, Milne, RL, Giles, GG, Manjer, J, Sandsveden, M, Langhammer, A, Sorgjerd, EP, Grankvist, K, Freedman, ND, Huang, W-Y, Chen, C, Prentice, R, Stevens, VL, Wang, Y, Le Marchand, L, Wilkens, LR, Weinstein, SJ, Albanes, D, Cai, Q, Blot, WJ, Arslan, AA, Zeleniuch-Jacquotte, A, Shu, X-O, Zheng, W, Yuan, J-M, Koh, W-P, Visvanathan, K, Sesso, HD, Zhang, X, Gaziano, JM, Fanidi, A, Muller, D, Brennan, P, Guida, F, and Robbins, HA
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Imbalances of blood biomarkers are associated with disease, and biomarkers may also vary non-pathologically across population groups. We described variation in concentrations of biomarkers of one-carbon metabolism, vitamin status, inflammation including tryptophan metabolism, and endothelial and renal function among cancer-free older adults. We analyzed 5167 cancer-free controls aged 40-80 years from 20 cohorts in the Lung Cancer Cohort Consortium (LC3). Centralized biochemical analyses of 40 biomarkers in plasma or serum were performed. We fit multivariable linear mixed effects models to quantify variation in standardized biomarker log-concentrations across four factors: age, sex, smoking status, and body mass index (BMI). Differences in most biomarkers across most factors were small, with 93% (186/200) of analyses showing an estimated difference lower than 0.25 standard-deviations, although most were statistically significant due to large sample size. The largest difference was for creatinine by sex, which was - 0.91 standard-deviations lower in women than men (95%CI - 0.98; - 0.84). The largest difference by age was for total cysteine (0.40 standard-deviation increase per 10-year increase, 95%CI 0.36; 0.43), and by BMI was for C-reactive protein (0.38 standard-deviation increase per 5-kg/m2 increase, 95%CI 0.34; 0.41). For 31 of 40 markers, the mean difference between current and never smokers was larger than between former and never smokers. A statistically significant (p < 0.05) association with time since smoking cessation was observed for 8 markers, including C-reactive protein, kynurenine, choline, and total homocysteine. We conclude that most blood biomarkers show small variations across demographic characteristics. Patterns by smoking status point to normalization of multiple physiological processes after smoking cessation.
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- 2021
236. Nongenetic Determinants of Risk for Early-Onset Colorectal Cancer
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Archambault, AN, Lin, Y, Jeon, J, Harrison, TA, Bishop, DT, Brenner, H, Casey, G, Chan, AT, Chang-Claude, J, Figueiredo, JC, Gallinger, S, Gruber, SB, Gunter, MJ, Hoffmeister, M, Jenkins, MA, Keku, TO, Le Marchand, L, Li, L, Moreno, V, Newcomb, PA, Pai, R, Parfrey, PS, Rennert, G, Sakoda, LC, Sandler, RS, Slattery, ML, Song, M, Win, AK, Woods, MO, Murphy, N, Campbell, PT, Su, Y-R, Zeleniuch-Jacquotte, A, Liang, PS, Du, M, Hsu, L, Peters, U, Hayes, RB, Archambault, AN, Lin, Y, Jeon, J, Harrison, TA, Bishop, DT, Brenner, H, Casey, G, Chan, AT, Chang-Claude, J, Figueiredo, JC, Gallinger, S, Gruber, SB, Gunter, MJ, Hoffmeister, M, Jenkins, MA, Keku, TO, Le Marchand, L, Li, L, Moreno, V, Newcomb, PA, Pai, R, Parfrey, PS, Rennert, G, Sakoda, LC, Sandler, RS, Slattery, ML, Song, M, Win, AK, Woods, MO, Murphy, N, Campbell, PT, Su, Y-R, Zeleniuch-Jacquotte, A, Liang, PS, Du, M, Hsu, L, Peters, U, and Hayes, RB
- Abstract
BACKGROUND: Incidence of early-onset (younger than 50 years of age) colorectal cancer (CRC) is increasing in many countries. Thus, elucidating the role of traditional CRC risk factors in early-onset CRC is a high priority. We sought to determine whether risk factors associated with late-onset CRC were also linked to early-onset CRC and whether association patterns differed by anatomic subsite. METHODS: Using data pooled from 13 population-based studies, we studied 3767 CRC cases and 4049 controls aged younger than 50 years and 23 437 CRC cases and 35 311 controls aged 50 years and older. Using multivariable and multinomial logistic regression, we estimated odds ratios (ORs) and 95% confidence intervals (CIs) to assess the association between risk factors and early-onset CRC and by anatomic subsite. RESULTS: Early-onset CRC was associated with not regularly using nonsteroidal anti-inflammatory drugs (OR = 1.43, 95% CI = 1.21 to 1.68), greater red meat intake (OR = 1.10, 95% CI = 1.04 to 1.16), lower educational attainment (OR = 1.10, 95% CI = 1.04 to 1.16), alcohol abstinence (OR = 1.23, 95% CI = 1.08 to 1.39), and heavier alcohol use (OR = 1.25, 95% CI = 1.04 to 1.50). No factors exhibited a greater excess in early-onset compared with late-onset CRC. Evaluating risks by anatomic subsite, we found that lower total fiber intake was linked more strongly to rectal (OR = 1.30, 95% CI = 1.14 to 1.48) than colon cancer (OR = 1.14, 95% CI = 1.02 to 1.27; P = .04). CONCLUSION: In this large study, we identified several nongenetic risk factors associated with early-onset CRC, providing a basis for targeted identification of those most at risk, which is imperative in mitigating the rising burden of this disease.
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- 2021
237. Hepcidin-regulating iron metabolism genes and pancreatic ductal adenocarcinoma: a pathway analysis of genome-wide association studies
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Julian-Serrano, S, Yuan, F, Wheeler, W, Benyamin, B, Machiela, MJ, Arslan, AA, Beane-Freeman, LE, Bracci, PM, Duell, EJ, Du, M, Gallinger, S, Giles, GG, Goodman, PJ, Kooperberg, C, Le Marchand, L, Neale, RE, Shu, X-O, Van den Eeden, SK, Visvanathan, K, Zheng, W, Albanes, D, Andreotti, G, Ardanaz, E, Babic, A, Berndt, S, Brais, LK, Brennan, P, Bueno-de-Mesquita, B, Buring, JE, Chanock, SJ, Childs, EJ, Chung, CC, Fabianova, E, Foretova, L, Fuchs, CS, Gaziano, JM, Gentiluomo, M, Giovannucci, EL, Goggins, MG, Hackert, T, Hartge, P, Hassan, MM, Holcatova, I, Holly, EA, Hung, R, Janout, V, Kurtz, RC, Lee, I-M, Malats, N, McKean, D, Milne, RL, Newton, CC, Oberg, AL, Perdomo, S, Peters, U, Porta, M, Rothman, N, Schulze, MB, Sesso, HD, Silverman, DT, Thompson, IM, Wactawski-Wende, J, Weiderpass, E, Wenstzensen, N, White, E, Wilkens, LR, Yu, H, Zeleniuch-Jacquotte, A, Zhong, J, Kraft, P, Li, D, Campbell, PT, Petersen, GM, Wolpin, BM, Risch, HA, Amundadottir, LT, Klein, AP, Yu, K, Stolzenberg-Solomon, RZ, Julian-Serrano, S, Yuan, F, Wheeler, W, Benyamin, B, Machiela, MJ, Arslan, AA, Beane-Freeman, LE, Bracci, PM, Duell, EJ, Du, M, Gallinger, S, Giles, GG, Goodman, PJ, Kooperberg, C, Le Marchand, L, Neale, RE, Shu, X-O, Van den Eeden, SK, Visvanathan, K, Zheng, W, Albanes, D, Andreotti, G, Ardanaz, E, Babic, A, Berndt, S, Brais, LK, Brennan, P, Bueno-de-Mesquita, B, Buring, JE, Chanock, SJ, Childs, EJ, Chung, CC, Fabianova, E, Foretova, L, Fuchs, CS, Gaziano, JM, Gentiluomo, M, Giovannucci, EL, Goggins, MG, Hackert, T, Hartge, P, Hassan, MM, Holcatova, I, Holly, EA, Hung, R, Janout, V, Kurtz, RC, Lee, I-M, Malats, N, McKean, D, Milne, RL, Newton, CC, Oberg, AL, Perdomo, S, Peters, U, Porta, M, Rothman, N, Schulze, MB, Sesso, HD, Silverman, DT, Thompson, IM, Wactawski-Wende, J, Weiderpass, E, Wenstzensen, N, White, E, Wilkens, LR, Yu, H, Zeleniuch-Jacquotte, A, Zhong, J, Kraft, P, Li, D, Campbell, PT, Petersen, GM, Wolpin, BM, Risch, HA, Amundadottir, LT, Klein, AP, Yu, K, and Stolzenberg-Solomon, RZ
- Abstract
BACKGROUND: Epidemiological studies have suggested positive associations for iron and red meat intake with risk of pancreatic ductal adenocarcinoma (PDAC). Inherited pathogenic variants in genes involved in the hepcidin-regulating iron metabolism pathway are known to cause iron overload and hemochromatosis. OBJECTIVES: The objective of this study was to determine whether common genetic variation in the hepcidin-regulating iron metabolism pathway is associated with PDAC. METHODS: We conducted a pathway analysis of the hepcidin-regulating genes using single nucleotide polymorphism (SNP) summary statistics generated from 4 genome-wide association studies in 2 large consortium studies using the summary data-based adaptive rank truncated product method. Our population consisted of 9253 PDAC cases and 12,525 controls of European descent. Our analysis included 11 hepcidin-regulating genes [bone morphogenetic protein 2 (BMP2), bone morphogenetic protein 6 (BMP6), ferritin heavy chain 1 (FTH1), ferritin light chain (FTL), hepcidin (HAMP), homeostatic iron regulator (HFE), hemojuvelin (HJV), nuclear factor erythroid 2-related factor 2 (NRF2), ferroportin 1 (SLC40A1), transferrin receptor 1 (TFR1), and transferrin receptor 2 (TFR2)] and their surrounding genomic regions (±20 kb) for a total of 412 SNPs. RESULTS: The hepcidin-regulating gene pathway was significantly associated with PDAC (P = 0.002), with the HJV, TFR2, TFR1, BMP6, and HAMP genes contributing the most to the association. CONCLUSIONS: Our results support that genetic susceptibility related to the hepcidin-regulating gene pathway is associated with PDAC risk and suggest a potential role of iron metabolism in pancreatic carcinogenesis. Further studies are needed to evaluate effect modification by intake of iron-rich foods on this association.
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- 2021
238. Breast Cancer Risk Factors and Circulating Anti-Müllerian Hormone Concentration in Healthy Premenopausal Women
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Clendenen, Tess V., Ge, Wenzhen, Koenig, Karen L., Afanasyeva, Yelena, Agnoli, Claudia, Bertone-Johnson, Elizabeth, Brinton, Louise A., Darvishian, Farbod, Dorgan, Joanne F., Eliassen, A. Heather, Falk, Roni T., Hallmans, Göran, Hankinson, Susan E., Hoffman-Bolton, Judith, Key, Timothy J., Krogh, Vittorio, Nichols, Hazel B., Sandler, Dale P., Schoemaker, Minouk J., Sluss, Patrick M., Sund, Malin, Swerdlow, Anthony J., Visvanathan, Kala, Liu, Mengling, Zeleniuch-Jacquotte, Anne, Clendenen, Tess V., Ge, Wenzhen, Koenig, Karen L., Afanasyeva, Yelena, Agnoli, Claudia, Bertone-Johnson, Elizabeth, Brinton, Louise A., Darvishian, Farbod, Dorgan, Joanne F., Eliassen, A. Heather, Falk, Roni T., Hallmans, Göran, Hankinson, Susan E., Hoffman-Bolton, Judith, Key, Timothy J., Krogh, Vittorio, Nichols, Hazel B., Sandler, Dale P., Schoemaker, Minouk J., Sluss, Patrick M., Sund, Malin, Swerdlow, Anthony J., Visvanathan, Kala, Liu, Mengling, and Zeleniuch-Jacquotte, Anne
- Abstract
Context: We previously reported that anti-Müllerian hormone (AMH), a marker of ovarian reserve, is positively associated with breast cancer risk, consistent with other studies. Objective: This study assessed whether risk factors for breast cancer are correlates of AMH concentration. Methods: This cross-sectional study included 3831 healthy premenopausal women (aged 21-57, 87% aged 35-49) from 10 cohort studies among the general population. Results: Adjusting for age and cohort, AMH positively associated with age at menarche (P < 0.0001) and parity (P = 0.0008) and inversely associated with hysterectomy/partial oophorectomy (P = 0.0008). Compared with women of normal weight, AMH was lower (relative geometric mean difference 27%, P < 0.0001) among women who were obese. Current oral contraceptive (OC) use and current/former smoking were associated with lower AMH concentration than never use (40% and 12% lower, respectively, P < 0.0001). We observed higher AMH concentrations among women who had had a benign breast biopsy (15% higher, P = 0.03), a surrogate for benign breast disease, an association that has not been reported. In analyses stratified by age (<40 vs ≥40), associations of AMH with body mass index and OCs were similar in younger and older women, while associations with the other factors (menarche, parity, hysterectomy/partial oophorectomy, smoking, and benign breast biopsy) were limited to women ≥40 (P-interaction < 0.05). Conclusion: This is the largest study of AMH and breast cancer risk factors among women from the general population (not presenting with infertility), and it suggests that most associations are limited to women over 40, who are approaching menopause and whose AMH concentration is declining.
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- 2021
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239. Dairy foods, calcium, and risk of breast cancer overall and for subtypes defined by estrogen receptor status : a pooled analysis of 21 cohort studies
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Wu, You, Huang, Ruyi, Wang, Molin, Bernstein, Leslie, Bethea, Traci N., Chen, Chu, Chen, Yu, Eliassen, A. Heather, Freedman, Neal D., Gaudet, Mia M., Gierach, Gretchen L., Giles, Graham G., Krogh, Vittorio, Larsson, Susanna C., Liao, Linda M., McCullough, Marjorie L., Miller, Anthony B., Milne, Roger L., Monroe, Kristine R., Neuhouser, Marian L., Palmer, Julie R., Prizment, Anna, Reynolds, Peggy, Robien, Kim, Rohan, Thomas E., Sandin, Sven, Sawada, Norie, Sieri, Sabina, Sinha, Rashmi, Stolzenberg-Solomon, Rachael Z., Tsugane, Shoichiro, van den Brandt, Piet A., Visvanathan, Kala, Weiderpass, Elisabete, Wilkens, Lynne R., Willett, Walter C., Wolk, Alicja, Zeleniuch-Jacquotte, Anne, Ziegler, Regina G., Smith-Warner, Stephanie A., Wu, You, Huang, Ruyi, Wang, Molin, Bernstein, Leslie, Bethea, Traci N., Chen, Chu, Chen, Yu, Eliassen, A. Heather, Freedman, Neal D., Gaudet, Mia M., Gierach, Gretchen L., Giles, Graham G., Krogh, Vittorio, Larsson, Susanna C., Liao, Linda M., McCullough, Marjorie L., Miller, Anthony B., Milne, Roger L., Monroe, Kristine R., Neuhouser, Marian L., Palmer, Julie R., Prizment, Anna, Reynolds, Peggy, Robien, Kim, Rohan, Thomas E., Sandin, Sven, Sawada, Norie, Sieri, Sabina, Sinha, Rashmi, Stolzenberg-Solomon, Rachael Z., Tsugane, Shoichiro, van den Brandt, Piet A., Visvanathan, Kala, Weiderpass, Elisabete, Wilkens, Lynne R., Willett, Walter C., Wolk, Alicja, Zeleniuch-Jacquotte, Anne, Ziegler, Regina G., and Smith-Warner, Stephanie A.
- Abstract
Background: Epidemiologic studies examining the relations between dairy product and calcium intakes and breast cancer have been inconclusive, especially for tumor subtypes. Objective: To evaluate the associations between intakes of specific dairy products and calcium and risk of breast cancer overall and for subtypes defined by estrogen receptor (ER) status. Method: We pooled the individual-level data of over 1 million women who were followed for a maximum of 8-20 years across studies. Associations were evaluated for dairy product and calcium intakes and risk of incident invasive breast cancer overall (n = 37,861 cases) and by subtypes defined by ER status. Study-specific multivariable hazard ratios (HRs) were estimated and then combined using random-effects models. Results: Overall, no clear association was observed between the consumption of specific dairy foods, dietary (from foods only) calcium, and total (from foods and supplements) calcium, and risk of overall breast cancer. Although each dairy product showed a null or very weak inverse association with risk of overall breast cancer (P, test for trend >0.05 for all), differences by ER status were suggested for yogurt and cottage/ricotta cheese with associations observed for ER-negative tumors only (pooled HR = 0.90, 95% CI: 0.83, 0.98 comparing >= 60 g/d with <1 g/d of yogurt and 0.85, 95% CI: 0.76, 0.95 comparing >= 25 g/d with <1 g/d of cottage/ricotta cheese). Dietary calcium intake was only weakly associated with breast cancer risk (pooled HR = 0.98, 95% CI: 0.97, 0.99 per 350 mg/d). Conclusion: Our study shows that adult dairy or calcium consumption is unlikely to associate with a higher risk of breast cancer and that higher yogurt and cottage/ricotta cheese intakes were inversely associated with the risk of ER-negative breast cancer, a less hormonally dependent subtype with poor prognosis. Future studies on fermented dairy products, earlier life exposures, ER-negative breast cancer, and di
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- 2021
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240. Epidemiology of 40 blood biomarkers of one-carbon metabolism, vitamin status, inflammation, and renal and endothelial function among cancer-free older adults
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Zahed, Hana, Johansson, Mattias, Ueland, Per M., Midttun, Øivind, Milne, Roger L., Giles, Graham G., Manjer, Jonas, Sandsveden, Malte, Langhammer, Arnulf, Sørgjerd, Elin Pettersen, Grankvist, Kjell, Johansson, Mikael, Freedman, Neal D., Huang, Wen-Yi, Chen, Chu, Prentice, Ross, Stevens, Victoria L., Wang, Ying, Le Marchand, Loic, Wilkens, Lynne R., Weinstein, Stephanie J., Albanes, Demetrius, Cai, Qiuyin, Blot, William J., Arslan, Alan A., Zeleniuch-Jacquotte, Anne, Shu, Xiao-Ou, Zheng, Wei, Yuan, Jian-Min, Koh, Woon-Puay, Visvanathan, Kala, Sesso, Howard D., Zhang, Xuehong, Gaziano, J. Michael, Fanidi, Anouar, Muller, David, Brennan, Paul, Guida, Florence, Robbins, Hilary A., Zahed, Hana, Johansson, Mattias, Ueland, Per M., Midttun, Øivind, Milne, Roger L., Giles, Graham G., Manjer, Jonas, Sandsveden, Malte, Langhammer, Arnulf, Sørgjerd, Elin Pettersen, Grankvist, Kjell, Johansson, Mikael, Freedman, Neal D., Huang, Wen-Yi, Chen, Chu, Prentice, Ross, Stevens, Victoria L., Wang, Ying, Le Marchand, Loic, Wilkens, Lynne R., Weinstein, Stephanie J., Albanes, Demetrius, Cai, Qiuyin, Blot, William J., Arslan, Alan A., Zeleniuch-Jacquotte, Anne, Shu, Xiao-Ou, Zheng, Wei, Yuan, Jian-Min, Koh, Woon-Puay, Visvanathan, Kala, Sesso, Howard D., Zhang, Xuehong, Gaziano, J. Michael, Fanidi, Anouar, Muller, David, Brennan, Paul, Guida, Florence, and Robbins, Hilary A.
- Abstract
Imbalances of blood biomarkers are associated with disease, and biomarkers may also vary non-pathologically across population groups. We described variation in concentrations of biomarkers of one-carbon metabolism, vitamin status, inflammation including tryptophan metabolism, and endothelial and renal function among cancer-free older adults. We analyzed 5167 cancer-free controls aged 40–80 years from 20 cohorts in the Lung Cancer Cohort Consortium (LC3). Centralized biochemical analyses of 40 biomarkers in plasma or serum were performed. We fit multivariable linear mixed effects models to quantify variation in standardized biomarker log-concentrations across four factors: age, sex, smoking status, and body mass index (BMI). Differences in most biomarkers across most factors were small, with 93% (186/200) of analyses showing an estimated difference lower than 0.25 standard-deviations, although most were statistically significant due to large sample size. The largest difference was for creatinine by sex, which was − 0.91 standard-deviations lower in women than men (95%CI − 0.98; − 0.84). The largest difference by age was for total cysteine (0.40 standard-deviation increase per 10-year increase, 95%CI 0.36; 0.43), and by BMI was for C-reactive protein (0.38 standard-deviation increase per 5-kg/m2 increase, 95%CI 0.34; 0.41). For 31 of 40 markers, the mean difference between current and never smokers was larger than between former and never smokers. A statistically significant (p < 0.05) association with time since smoking cessation was observed for 8 markers, including C-reactive protein, kynurenine, choline, and total homocysteine. We conclude that most blood biomarkers show small variations across demographic characteristics. Patterns by smoking status point to normalization of multiple physiological processes after smoking cessation.
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- 2021
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241. Prolactin and risk of epithelial ovarian cancer
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Hathaway, Cassandra A., Rice, Megan S., Townsend, Mary K., Hankinson, Susan E., Arslan, Alan A., Buring, Julie E., Hallmans, Göran, Idahl, Annika, Kubzansky, Laura D., Lee, I-Min, Lundin, Eva, Sluss, Patrick M., Zeleniuch-Jacquotte, Anne, Tworoger, Shelley S., Hathaway, Cassandra A., Rice, Megan S., Townsend, Mary K., Hankinson, Susan E., Arslan, Alan A., Buring, Julie E., Hallmans, Göran, Idahl, Annika, Kubzansky, Laura D., Lee, I-Min, Lundin, Eva, Sluss, Patrick M., Zeleniuch-Jacquotte, Anne, and Tworoger, Shelley S.
- Abstract
Background: Prolactin is synthesized in the ovaries and may play a role in ovarian cancer etiology. One prior prospective study observed a suggestive positive association between prolactin levels and risk of ovarian cancer. Methods: Weconducted a pooled case-control study of 703 cases and 864 matched controls nested within five prospective cohorts. We used unconditional logistic regression to calculate adjusted odds ratios (OR) and 95% confidence intervals (CI) for the association between prolactin and ovarian cancer risk. We examined heterogeneity by menopausal status at blood collection, body mass index (BMI), age, and histotype. Results: Among women with known menopausal status, we observed a positive trend in the association between prolactin and ovarian cancer risk (Ptrend = 0.045; OR, quartile 4 vs. 1 = 1.34; 95% CI = 0.97–1.85), but no significant association was observed for premenopausal or postmenopausal women individually (corresponding OR = 1.38; 95% CI = 0.74–2.58; Ptrend = 0.32 and OR = 1.41; 95% CI = 0.93–2.13; Ptrend = 0.08, respectively; Pheterogeneity = 0.91). In stratified analyses, we observed a positive association between prolactin and risk for women with BMI ≥ 25 kg/m2, but not BMI < 25 kg/m2 (corresponding OR = 2.68; 95% CI = 1.56–4.59; Ptrend < 0.01 and OR = 0.90; 95% CI = 0.58–1.40; Ptrend = 0.98, respectively; Pheterogeneity < 0.01). Associations did not vary by age, postmenopausal hormone therapy use, histotype, or time between blood draw and diagnosis. Conclusions: We found a trend between higher prolactin levels and increased ovarian cancer risk, especially among women with a BMI ≥ 25 kg/m2. Impact: This work supports a previous study linking higher prolactin with ovarian carcinogenesis in a high adiposity setting. Future work is needed to understand the mechanism underlying this association.
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- 2021
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242. Dairy foods, calcium, and risk of breast cancer overall and for subtypes defined by estrogen receptor status: a pooled analysis of 21 cohort studies
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Wu, Y., Huang, R.Y., Wang, M.L., Bernstein, L., Bethea, T.N., Chen, C., Chen, Y., Eliassen, A.H., Freedman, N.D., Gaudet, M.M., Gierach, G.L., Giles, G.G., Krogh, V., Larsson, S.C., Liao, L.M., McCullough, M.L., Miller, A.B., Milne, R.L., Monroe, K.R., Neuhouser, M.L., Palmer, J.R., Prizment, A., Reynolds, P., Robien, K., Rohan, T.E., Sandin, S., Sawada, N., Sieri, S., Sinha, R., Stolzenberg-Solomon, R.Z., Tsugane, S., van den Brandt, P.A., Visvanathan, K., Weiderpass, E., Wilkens, L.R., Willett, W.C., Wolk, A., Zeleniuch-Jacquotte, A., Ziegler, R.G., Smith-Warner, S.A., Wu, Y., Huang, R.Y., Wang, M.L., Bernstein, L., Bethea, T.N., Chen, C., Chen, Y., Eliassen, A.H., Freedman, N.D., Gaudet, M.M., Gierach, G.L., Giles, G.G., Krogh, V., Larsson, S.C., Liao, L.M., McCullough, M.L., Miller, A.B., Milne, R.L., Monroe, K.R., Neuhouser, M.L., Palmer, J.R., Prizment, A., Reynolds, P., Robien, K., Rohan, T.E., Sandin, S., Sawada, N., Sieri, S., Sinha, R., Stolzenberg-Solomon, R.Z., Tsugane, S., van den Brandt, P.A., Visvanathan, K., Weiderpass, E., Wilkens, L.R., Willett, W.C., Wolk, A., Zeleniuch-Jacquotte, A., Ziegler, R.G., and Smith-Warner, S.A.
- Abstract
Background: Epidemiologic studies examining the relations between dairy product and calcium intakes and breast cancer have been inconclusive, especially for tumor subtypes.Objective: To evaluate the associations between intakes of specific dairy products and calcium and risk of breast cancer overall and for subtypes defined by estrogen receptor (ER) status.Method: We pooled the individual-level data of over 1 million women who were followed for a maximum of 8-20 years across studies. Associations were evaluated for dairy product and calcium intakes and risk of incident invasive breast cancer overall (n = 37,861 cases) and by subtypes defined by ER status. Study-specific multivariable hazard ratios (HRs) were estimated and then combined using random-effects models.Results: Overall, no clear association was observed between the consumption of specific dairy foods, dietary (from foods only) calcium, and total (from foods and supplements) calcium, and risk of overall breast cancer. Although each dairy product showed a null or very weak inverse association with risk of overall breast cancer (P, test for trend >0.05 for all), differences by ER status were suggested for yogurt and cottage/ricotta cheese with associations observed for ER-negative tumors only (pooled HR = 0.90, 95% CI: 0.83, 0.98 comparing >= 60 g/d with = 25 g/d withConclusion: Our study shows that adult dairy or calcium consumption is unlikely to associate with a higher risk of breast cancer and that higher yogurt and cottage/ricotta cheese intakes were inversely associated with the risk of ER-negative breast cancer, a less hormonally dependent subtype with poor prognosis. Future studies on fermented dairy products, earlier life exposures, ER-negative breast cancer, and different racial/ethnic populations may further elucidate the relation.
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- 2021
243. Smoking Modifies Pancreatic Cancer Risk Loci on 2q21.3
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Mocci, Evelina, Kundu, Prosenjit, Wheeler, William, Arslan, Alan A., Beane-Freeman, Laura E., Bracci, Paige M., Brennan, Paul, Canzian, Federico, Du, Mengmeng, Gallinger, Steven, Giles, Graham G., Goodman, Phyllis J., Kooperberg, Charles, Le Marchand, Loic, Neale, Rachel E., Shu, Xiao-Ou, Visvanathan, Kala, White, Emily, Zheng, Wei, Albanes, Demetrius, Andreotti, Gabriella, Babic, Ana, Bamlet, William R., Berndt, Sonja, Blackford, Amanda L., Bueno-de-Mesquita, Bas, Buring, Julie E., Campa, Daniele, Chanock, Stephen J., Childs, Erica J., Duell, Eric J., Fuchs, Charles S., Gaziano, J. Michael, Giovannucci, Edward L., Goggins, Michael G., Hartge, Patricia, Hassan, Manal M., Holly, Elizabeth A., Hoover, Robert N., Hung, Rayjean J., Kurtz, Robert C., Lee, I-Min, Malats, Nuria, Milne, Roger L., Ng, Kimmie, Oberg, Ann L., Panico, Salvatore, Peters, Ulrike, Porta, Miquel, Rabe, Kari G., Riboli, Elio, Rothman, Nathaniel, Scelo, Ghislaine, Sesso, Howard D., Silverman, Debra T., Stevens, Victoria L., Strobel, Oliver, Thompson, Ian M., Tjonneland, Anne, Trichopoulou, Antonia, Van den Eeden, Stephen K., Wactawski-Wende, Jean, Wentzensen, Nicolas, Wilkens, Lynne R., Yu, Herbert, Yuan, Fangcheng, Zeleniuch-Jacquotte, Anne, Amundadottir, Laufey T., Li, Donghui, Jacobs, Eric J., Petersen, Gloria M., Wolpin, Brian M., Risch, Harvey A., Kraft, Peter, Chatterjee, Nilanjan, Klein, Alison P., Stolzenberg-Solomon, Rachael, Mocci, Evelina, Kundu, Prosenjit, Wheeler, William, Arslan, Alan A., Beane-Freeman, Laura E., Bracci, Paige M., Brennan, Paul, Canzian, Federico, Du, Mengmeng, Gallinger, Steven, Giles, Graham G., Goodman, Phyllis J., Kooperberg, Charles, Le Marchand, Loic, Neale, Rachel E., Shu, Xiao-Ou, Visvanathan, Kala, White, Emily, Zheng, Wei, Albanes, Demetrius, Andreotti, Gabriella, Babic, Ana, Bamlet, William R., Berndt, Sonja, Blackford, Amanda L., Bueno-de-Mesquita, Bas, Buring, Julie E., Campa, Daniele, Chanock, Stephen J., Childs, Erica J., Duell, Eric J., Fuchs, Charles S., Gaziano, J. Michael, Giovannucci, Edward L., Goggins, Michael G., Hartge, Patricia, Hassan, Manal M., Holly, Elizabeth A., Hoover, Robert N., Hung, Rayjean J., Kurtz, Robert C., Lee, I-Min, Malats, Nuria, Milne, Roger L., Ng, Kimmie, Oberg, Ann L., Panico, Salvatore, Peters, Ulrike, Porta, Miquel, Rabe, Kari G., Riboli, Elio, Rothman, Nathaniel, Scelo, Ghislaine, Sesso, Howard D., Silverman, Debra T., Stevens, Victoria L., Strobel, Oliver, Thompson, Ian M., Tjonneland, Anne, Trichopoulou, Antonia, Van den Eeden, Stephen K., Wactawski-Wende, Jean, Wentzensen, Nicolas, Wilkens, Lynne R., Yu, Herbert, Yuan, Fangcheng, Zeleniuch-Jacquotte, Anne, Amundadottir, Laufey T., Li, Donghui, Jacobs, Eric J., Petersen, Gloria M., Wolpin, Brian M., Risch, Harvey A., Kraft, Peter, Chatterjee, Nilanjan, Klein, Alison P., and Stolzenberg-Solomon, Rachael
- Abstract
Germline variation and smoking are independently associated with pancreatic ductal adenocarcinoma (PDAC). We conducted genome-wide smoking interaction analysis of PDAC using genotype data from four previous genome-wide association studies in individuals of European ancestry (7,937 cases and 11,774 controls). Examination of expression quantitative trait loci data from the Genotype-Tissue Expression Project followed by colocalization analysis was conducted to determine whether there was support for common SNP(s) underlying the observed associations. Statistical tests were two sided and P < 5 similar to 10(-8) was considered statistically significant. Genome-wide significant evidence of qualitative interaction was identified on chr2q21.3 in intron 5 of the transmembrane protein 163 (TMEM163) and upstream of the cyclin T2 (CCNT2). The most significant SNP using the Empirical Bayes method, in this region that included 45 significantly associated SNPs, was rs1818613 [per allele OR in never smokers 0.87, 95% confidence interval (CI), 0.82-0.93; former smokers 1.00, 95% CI, 0.91-1.07; current smokers 1.25, 95% CI 1.12-1.40, P-interaction = 3.08 x 10(-9)). Examination of the Genotype-Tissue Expression Project data demonstrated an expression quantitative trait locus in this region for TMEM163 and CCNT2 in several tissue types. Colocalization analysis supported a shared SNP, rs842357, in high linkage disequilibrium with rs1818613 (r(2) = 0. 94) driving both the observed interaction and the expression quantitative trait loci signals. Future studies are needed to confirm and understand the differential biologic mechanisms by smoking status that contribute to our PDAC findings.Significance: This large genome-wide interaction study identifies a susceptibility locus on 2q21.3 that significantly modified PDAC risk by smoking status, providing insight into smoking-associated PDAC, with implications for prevention.
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- 2021
244. Serum prohepcidin is associated with soluble transferrin receptor-1 but not ferritin in healthy post-menopausal women
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Huang, Xi, Fung, Eric T., Yip, Christine, and Zeleniuch-Jacquotte, Anne
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- 2008
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245. Vitamin D receptor polymorphisms and risk of epithelial ovarian cancer
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Clendenen, Tess V., Arslan, Alan A., Koenig, Karen L., Enquist, Kerstin, Wirgin, Isaac, Ågren, Åsa, Lukanova, Annekatrin, Sjodin, Hubert, Zeleniuch-Jacquotte, Anne, Shore, Roy E., Hallmans, Göran, Toniolo, Paolo, and Lundin, Eva
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- 2008
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246. Alcohol intake and pancreatic cancer: a pooled analysis from the pancreatic cancer cohort consortium (PanScan)
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Michaud, Dominique S., Vrieling, Alina, Jiao, Li, Mendelsohn, Julie B., Steplowski, Emily, Lynch, Shannon M., Wactawski-Wende, Jean, Arslan, Alan A., Bas Bueno-de-Mesquita, H., Fuchs, Charles S., Gross, Myron, Helzlsouer, Kathy, Jacobs, Eric J., LaCroix, Andrea, Petersen, Gloria, Zheng, Wei, Allen, Naomi, Ammundadottir, Laufey, Bergmann, Manuela M., Boffetta, Paolo, Buring, Julie E., Canzian, Federico, Chanock, Stephen J., Clavel-Chapelon, Françoise, Clipp, Sandra, Freiberg, Matthew S., Michael Gaziano, J., Giovannucci, Edward L., Hankinson, Susan, Hartge, Patricia, Hoover, Robert N., Allan Hubbell, F., Hunter, David J., Hutchinson, Amy, Jacobs, Kevin, Kooperberg, Charles, Kraft, Peter, Manjer, Jonas, Navarro, Carmen, Peeters, Petra H. M., Shu, Xiao-Ou, Stevens, Victoria, Thomas, Gilles, Tjønneland, Anne, Tobias, Geoffrey S., Trichopoulos, Dimitrios, Tumino, Rosario, Vineis, Paolo, Virtamo, Jarmo, Wallace, Robert, Wolpin, Brian M., Yu, Kai, Zeleniuch-Jacquotte, Anne, and Stolzenberg-Solomon, Rachael Z.
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- 2010
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247. IGF-I during primiparous pregnancy and maternal risk of breast cancer
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Chen, Tianhui, Lukanova, Annekatrin, Grankvist, Kjell, Zeleniuch-Jacquotte, Anne, Wulff, Marianne, Johansson, Robert, Schock, Helena, Lenner, Per, Hallmans, Goran, Wadell, Goran, Toniolo, Paolo, and Lundin, Eva
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- 2010
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248. Body-mass index and mortality among 1.46 million white adults
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de Gonzalez, Amy Berrington, Hartge, Patricia, Cerhan, James R., Flint, Alan J., Hannan, Lindsay, MacInnis, Robert J., Moore, Steven C., Tobias, Geoffrey S., Anton-Culver, Hoda, Freeman, Laura Beane, Beeson, W. Lawrence, Clipp, Sandra L., English, Dallas R., Folsom, Aaron R., Freedman, Michal, Giles, Graham, Hakansson, Niclas, Henderson, Katherine D., Hoffman-Bolton, Judith, Hoppin, Jane A., Koenig, Karen L., I-Min Lee, Linet, Martha S., Yikyung Park, Sesso, Howard D., Weiderpass, Elisabete, Willcox, Bradley J., Pocobelli, Gaia, Schatzkin, Arthur, Wolk, Alicja, Zeleniuch-Jacquotte, Anne, Willett, Walter C., and Thun, Michael J.
- Subjects
Mortality -- United States ,Mortality -- Risk factors ,Obesity -- Risk factors ,Body mass index -- Measurement ,Body mass index -- Health aspects - Abstract
The optimal body-mass index (BMI) range is assessed and has provided stable estimates of the risks associated with being overweight, obese, and morbidly obese, with minimal confounding due to smoking or prevalent disease. The studies have shown that for non-Hispanic whites, both overweight and obesity are associated with increased all-cause mortality and also underweight.
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- 2010
249. Body size and multiple myeloma mortality: a pooled analysis of 20 prospective studies
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Teras, Lauren R., Kitahara, Cari M., Birmann, Brenda M., Hartge, Patricia A., Wang, Sophia S., Robien, Kim, Patel, Alpa V., Adami, Hans-Olov, Weiderpass, Elisabete, Giles, Graham G., Singh, Pramil N., Alavanja, Michael, Beane Freeman, Laura E., Bernstein, Leslie, Buring, Julie E., Colditz, Graham A., Fraser, Gary E., Gapstur, Susan M., Gaziano, Michael J., Giovannucci, Edward, Hofmann, Jonathan N., Linet, Martha S., Neta, Gila, Park, Yikyung, Peters, Ulrike, Rosenberg, Philip S., Schairer, Catherine, Sesso, Howard D., Stampfer, Meir J., Visvanathan, Kala, White, Emily, Wolk, Alicja, Zeleniuch-Jacquotte, Anne, de González, Amy Berrington, and Purdue, Mark P.
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- 2014
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250. Genome-wide association study of survival in patients with pancreatic adenocarcinoma
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Wu, Chen, Kraft, Peter, Stolzenberg-Solomon, Rachael, Steplowski, Emily, Brotzman, Michelle, Xu, Mousheng, Mudgal, Poorva, Amundadottir, Laufey, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Gross, Myron, Helzlsouer, Kathy, Jacobs, Eric J, Kooperberg, Charles, Petersen, Gloria M, Zheng, Wei, Albanes, Demetrius, Boutron-Ruault, Marie-Christine, Buring, Julie E, Canzian, Federico, Cao, Guangwen, Duell, Eric J, Elena, Joanne W, Gaziano, J Michael, Giovannucci, Edward L, Hallmans, Goran, Hutchinson, Amy, Hunter, David J, Jenab, Mazda, Jiang, Guoliang, Khaw, Kay-Tee, LaCroix, Andrea, Li, Zhaoshen, Mendelsohn, Julie B, Panico, Salvatore, Patel, Alpa V, Qian, Zhi Rong, Riboli, Elio, Sesso, Howard, Shen, Hongbing, Shu, Xiao-Ou, Tjonneland, Anne, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Virtamo, Jarmo, Visvanathan, Kala, Wactawski-Wende, Jean, Wang, Chengfeng, Yu, Kai, Zeleniuch-Jacquotte, Anne, Chanock, Stephen, Hoover, Robert, Hartge, Patricia, Fuchs, Charles S, Lin, Dongxin, and Wolpin, Brian M
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- 2014
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