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Pancreatic Neoplasms: HELP
Articles by Thomas E. Rohan
Based on 11 articles published since 2010
(Why 11 articles?)
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Between 2010 and 2020, T. E. Rohan wrote the following 11 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Dairy products and pancreatic cancer risk: a pooled analysis of 14 cohort studies. 2014

Genkinger, J M / Wang, M / Li, R / Albanes, D / Anderson, K E / Bernstein, L / van den Brandt, P A / English, D R / Freudenheim, J L / Fuchs, C S / Gapstur, S M / Giles, G G / Goldbohm, R A / Håkansson, N / Horn-Ross, P L / Koushik, A / Marshall, J R / McCullough, M L / Miller, A B / Robien, K / Rohan, T E / Schairer, C / Silverman, D T / Stolzenberg-Solomon, R Z / Virtamo, J / Willett, W C / Wolk, A / Ziegler, R G / Smith-Warner, S A. ·Department of Epidemiology, Mailman School of Public Health, Columbia University, New York jg3081@columbia.edu. · Department of Epidemiology, Harvard School of Public Health, Boston Department of Biostatistics, Harvard School of Public Health, Boston. · Department of Epidemiology, Harvard School of Public Health, Boston. · Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda. · Division of Epidemiology and Community Health, School of Public Health, Masonic Cancer Center, University of Minnesota, Minneapolis. · Division of Cancer Etiology, Department of Population Science, Beckman Research Institute and City of Hope National Medical Center, Duarte, USA. · Department of Epidemiology, School for Oncology and Developmental Biology (GROW), Maastricht University, Maastricht, The Netherlands. · Cancer Epidemiology Centre, Cancer Council of Victoria, Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Melbourne, Australia. · Department of Social and Preventive Medicine, University at Buffalo, State University of New York, Buffalo. · Division of Medical Oncology, Dana-Farber Cancer Institute, Boston Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston. · Epidemiology Research Program, American Cancer Society, Atlanta, USA. · Department of Prevention and Health, TNO Quality of Life, Leiden, The Netherlands. · Division of Nutritional Epidemiology, National Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden. · Cancer Prevention Institute of California, Fremont, USA. · Department of Social and Preventive Medicine, University of Montreal, Montreal. · Dalla Lana School of Public Health, University of Toronto, Toronto, Canada. · Department of Epidemiology and Biostatistics, School of Public Health and Health Services, George Washington University, Washington, DC. · Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, USA. · Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland. · Department of Epidemiology, Harvard School of Public Health, Boston Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston Department of Nutrition, Harvard School of Public Health, Boston, USA. · Department of Epidemiology, Harvard School of Public Health, Boston Department of Nutrition, Harvard School of Public Health, Boston, USA. ·Ann Oncol · Pubmed #24631943.

ABSTRACT: Pancreatic cancer has few early symptoms, is usually diagnosed at late stages, and has a high case-fatality rate. Identifying modifiable risk factors is crucial to reducing pancreatic cancer morbidity and mortality. Prior studies have suggested that specific foods and nutrients, such as dairy products and constituents, may play a role in pancreatic carcinogenesis. In this pooled analysis of the primary data from 14 prospective cohort studies, 2212 incident pancreatic cancer cases were identified during follow-up among 862 680 individuals. Adjusting for smoking habits, personal history of diabetes, alcohol intake, body mass index (BMI), and energy intake, multivariable study-specific hazard ratios (MVHR) and 95% confidence intervals (CIs) were calculated using the Cox proportional hazards models and then pooled using a random effects model. There was no association between total milk intake and pancreatic cancer risk (MVHR = 0.98, 95% CI = 0.82-1.18 comparing ≥500 with 1-69.9 g/day). Similarly, intakes of low-fat milk, whole milk, cheese, cottage cheese, yogurt, and ice-cream were not associated with pancreatic cancer risk. No statistically significant association was observed between dietary (MVHR = 0.96, 95% CI = 0.77-1.19) and total calcium (MVHR = 0.89, 95% CI = 0.71-1.12) intake and pancreatic cancer risk overall when comparing intakes ≥1300 with <500 mg/day. In addition, null associations were observed for dietary and total vitamin D intake and pancreatic cancer risk. Findings were consistent within sex, smoking status, and BMI strata or when the case definition was limited to pancreatic adenocarcinoma. Overall, these findings do not support the hypothesis that consumption of dairy foods, calcium, or vitamin D during adulthood is associated with pancreatic cancer risk.

2 Review Folate intake and risk of pancreatic cancer: pooled analysis of prospective cohort studies. 2011

Bao, Ying / Michaud, Dominique S / Spiegelman, Donna / Albanes, Demetrius / Anderson, Kristin E / Bernstein, Leslie / van den Brandt, Piet A / English, Dallas R / Freudenheim, Jo L / Fuchs, Charles S / Giles, Graham G / Giovannucci, Edward / Goldbohm, R Alexandra / Håkansson, Niclas / Horn-Ross, Pamela L / Jacobs, Eric J / Kitahara, Cari M / Marshall, James R / Miller, Anthony B / Robien, Kim / Rohan, Thomas E / Schatzkin, Arthur / Stevens, Victoria L / Stolzenberg-Solomon, Rachael Z / Virtamo, Jarmo / Wolk, Alicja / Ziegler, Regina G / Smith-Warner, Stephanie A. ·Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA. ·J Natl Cancer Inst · Pubmed #22034634.

ABSTRACT: BACKGROUND: Epidemiological studies evaluating the association between folate intake and risk of pancreatic cancer have produced inconsistent results. The statistical power to examine this association has been limited in previous studies partly because of small sample size and limited range of folate intake in some studies. METHODS: We analyzed primary data from 14 prospective cohort studies that included 319,716 men and 542,948 women to assess the association between folate intake and risk of pancreatic cancer. Folate intake was assessed through a validated food-frequency questionnaire at baseline in each study. Study-specific relative risks (RRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models and then pooled using a random effects model. All statistical tests were two-sided. RESULTS: During 7-20 years of follow-up across studies, 2195 pancreatic cancers were identified. No association was observed between folate intake and risk of pancreatic cancer in men and women (highest vs lowest quintile: dietary folate intake, pooled multivariable RR = 1.06, 95% CI = 0.90 to 1.25, P(trend) = .47; total folate intake [dietary folate and supplemental folic acid], pooled multivariable RR = 0.96, 95% CI = 0.80 to 1.16, P(trend) = .90). No between-study heterogeneity was observed (for dietary folate, P(heterogeneity) = .15; for total folate, P(heterogeneity) = .22). CONCLUSION: Folate intake was not associated with overall risk of pancreatic cancer in this large pooled analysis.

3 Article Adiposity, history of diabetes, and risk of pancreatic cancer in postmenopausal women. 2019

Arthur, Rhonda / Kabat, Geoffrey C / Kim, Mimi Y / Ho, Gloria Y F / Chlebowski, Rowan T / Pan, Kathy / Rohan, Thomas E. ·Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY. Electronic address: Rhonda.arthur@einstein.yu.edu. · New Rochelle, NY. · Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY. · Center for Health Innovations and Outcomes Research, Feinstein Institute for Medical Research, Northwell Health, Great Neck, NY. · Department of Medical Oncology and Therapeutics Research, City of Hope National Medical Center, Duarte, CA. · Department of Medical Oncology and Therapeutics Research, City of Hope National Medical Center, Duarte, CA; Department of Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA. ·Ann Epidemiol · Pubmed #30449532.

ABSTRACT: PURPOSE: The purpose of this study was to examine the association of type II diabetes and anthropometric variables with risk of pancreatic cancer among postmenopausal women. METHODS: Weight, height, waist circumference, and hip circumference were measured by trained personnel, whereas history of diabetes and weight earlier in life were self-reported. Pancreatic cancer was ascertained via central review of medical records by physician adjudicators. After exclusions, 1045 cases of pancreatic cancer were diagnosed among 156,218 women over a median follow-up of approximately 18 years. Cox proportional hazards models were used to estimate the associations of study factors with pancreatic cancer risk. RESULTS: Diabetes (hazards ratio (HR): 1.30; 95% confidence intervals (95% CI): 1.01-1.66), and in particular, waist circumference, waist-to-hip ratio, and waist-to-height ratio showed positive associations with pancreatic cancer risk (HRs for highest vs. lowest level 1.38; 95% CI: 1.14-1.66, 1.40; 1.17-1.68; and 1.36; 1.13-1.64, respectively). Body mass index at the baseline showed only a borderline positive association with risk (HR: 1.21; 95% CI: 0.97-1.51). Body mass index at age 50 years, but not at ages 18 and 35 years, was also associated with increased pancreatic cancer risk. CONCLUSIONS: In this study of postmenopausal women, central adiposity and, to a lesser extent, general adiposity and a history of diabetes, were associated with increased pancreatic cancer risk.

4 Article A prospective study of soluble receptor for advanced glycation end products and adipokines in association with pancreatic cancer in postmenopausal women. 2018

White, Donna L / Hoogeveen, Ron C / Chen, Liang / Richardson, Peter / Ravishankar, Milan / Shah, Preksha / Tinker, Lesley / Rohan, Thomas / Whitsel, Eric A / El-Serag, Hashem B / Jiao, Li. ·Department of Medicine, Baylor College of Medicine, Houston, Texas. · Center for Innovations in Quality, Effectiveness and Safety (IQuESt), Michael E. DeBakey VA Medical Center, Houston, Texas. · Texas Medical Center Digestive Disease Center, Houston, Texas. · Dan L. Duncan Cancer Center at Baylor College of Medicine, Houston, Texas. · Center for Translational Research on Inflammatory Diseases (CTRID), Michael E. DeBakey VA Medical Center, Houston, Texas. · Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington. · Albert Einstein College of Medicine, Bronx, New York. · Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. ·Cancer Med · Pubmed #29573228.

ABSTRACT: Advanced glycation end products (AGEs) dysregulate adipokines and induce inflammation by binding to their adipocyte receptor (RAGE). Soluble RAGE (sRAGE) prevents AGEs/RAGE signaling. We performed a nested case-control study of the association between sRAGE, adipokines, and incident pancreatic cancer risk in the prospective Women's Health Initiative Study. We individually matched controls (n = 802) to cases (n = 472) on age, race, and blood draw date. We evaluated serum concentrations of sRAGE, adiponectin, leptin, monocyte chemotactic protein 1 (MCP1), and plasminogen activator inhibitor-1 (PAI1) using immunoassay. We used conditional logistic regression model to estimate adjusted odds ratios (aORs) and 95% confidence intervals (CIs) for pancreatic cancer over biomarker quartiles (Q1-Q4). We used principal component analysis to create two composite biomarkers and performed a confirmatory factor analysis to examine the association between composite biomarker scores (CBS) and pancreatic cancer risk. Baseline serum sRAGE concentrations were inversely associated with pancreatic cancer risk (aOR

5 Article Reproductive factors, exogenous hormone use, and risk of pancreatic cancer in postmenopausal women. 2017

Kabat, Geoffrey C / Kamensky, Victor / Rohan, Thomas E. ·Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY 10461, United States. Electronic address: Geoffrey.kabat@einstein.yu.edu. · Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY 10461, United States. ·Cancer Epidemiol · Pubmed #28521283.

ABSTRACT: INTRODUCTION: The epidemiologic literature on menstrual and reproductive factors associated with pancreatic cancer has yielded weak and inconsistent evidence of an association. Furthermore, few cohort studies have examined the association of exogenous hormone use, including type and duration, with this disease. The aim of this study was to assess the association of these exposures with risk of pancreatic cancer in a large cohort of postmenopausal women. METHODS: We used data from the Women's Health Initiative on 1003 cases of pancreatic cancer diagnosed among 158,298 participants over 14.3 years of follow-up. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% confidence intervals (95% CI) for the associations of interest. RESULTS: Being parous vs. nulliparous was associated with reduced risk (HR=0.84, 95% CI 0.70-1.00), and women who had 1-2 and 3-4 births were at decreased risk compared to nulliparous women, whereas women who had >5 births showed no decrease in risk. Compared to women who gave birth between the ages of 20-29, women who gave birth at age 30 or above were at increased risk (HR 1.23, 95% CI 1.00-1.53, p for trend 0.003). Other reproductive factors and exogenous hormone use were not associated with risk. CONCLUSIONS: Together with the existing literature on this topic, our results suggest that reproductive and hormonal exposures are unlikely to play an important role in the etiology of pancreatic cancer.

6 Article Leucocyte telomere length, genetic variants at the 2017

Bao, Ying / Prescott, Jennifer / Yuan, Chen / Zhang, Mingfeng / Kraft, Peter / Babic, Ana / Morales-Oyarvide, Vicente / Qian, Zhi Rong / Buring, Julie E / Cochrane, Barbara B / Gaziano, J Michael / Giovannucci, Edward L / Manson, JoAnn E / Ng, Kimmie / Ogino, Shuji / Rohan, Thomas E / Sesso, Howard D / Stampfer, Meir J / Fuchs, Charles S / De Vivo, Immaculata / Amundadottir, Laufey T / Wolpin, Brian M. ·Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA. · Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA. · Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA. · Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. · Department of Biostatistics, Harvard School of Public Health, Boston, Massachusetts, USA. · Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA. · Department of Ambulatory Care and Prevention, Harvard Medical School, Boston, Massachusetts, USA. · University of Washington School of Nursing, Seattle, Washington, USA. · Massachusetts Veterans Epidemiology Research and Information Center (MAVERIC), VA Boston Healthcare System. · Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA. · Division of MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA. · Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, New York, USA. · Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts, USA. ·Gut · Pubmed #27797938.

ABSTRACT: OBJECTIVE: Telomere shortening occurs as an early event in pancreatic tumorigenesis, and genetic variants at the telomerase reverse transcriptase ( DESIGN: We measured prediagnostic leucocyte telomere length in 386 pancreatic cancer cases and 896 matched controls from five prospective US cohorts. ORs and 95% CIs were calculated using conditional logistic regression. Matching factors included year of birth, cohort (which also matches on sex), smoking status, fasting status and month/year of blood collection. We additionally examined single-nucleotide polymorphisms (SNPs) at the RESULTS: Shorter prediagnostic leucocyte telomere length was associated with higher risk of pancreatic cancer (comparing extreme quintiles of telomere length, OR 1.72; 95% CI 1.07 to 2.78; p CONCLUSIONS: Prediagnostic leucocyte telomere length and genetic variants at the

7 Article Prospective analysis of association between statins and pancreatic cancer risk in the Women's Health Initiative. 2016

Simon, Michael S / Desai, Pinkal / Wallace, Robert / Wu, Chunyuan / Howard, Barbara V / Martin, Lisa W / Schlecht, Nicolas / Liu, Simin / Jay, Allison / LeBlanc, Erin S / Rohan, Thomas / Manson, JoAnn. ·Department of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA. simonm@karmanos.org. · Barbara Ann Karmanos Cancer Institute, 4100 John R, 4221 HWCRC, Detroit, MI, USA. simonm@karmanos.org. · Weill Cornell Medical College, New York, NY, USA. · Department of Epidemiology, University of Iowa College of Public Health, Iowa City, IA, USA. · Fred Hutchinson Cancer Research Center, Seattle, WA, USA. · MedStar Health Research Institute and Georgetown/Howard Universities Center for Clinical and Translational Sciences, Washington, DC, USA. · George Washington University, Washington, DC, USA. · Albert Einstein College of Medicine, Bronx, NY, USA. · UCLA School of Public Health, Los Angeles, CA, USA. · St John's Hospital and Medical Center, Detroit, MI, USA. · Center for Health Research, Kaiser Permanente NW, Portland, OR, USA. · Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. ·Cancer Causes Control · Pubmed #26857832.

ABSTRACT: PURPOSE: To determine whether HMG-CoA reductase inhibitors (statins) are associated with a lower risk of pancreatic cancer. METHODS: The population included 160,578 postmenopausal women enrolled in the Women's Health Initiative (WHI) in which 385 incident cases of pancreatic cancer were identified over an average of 8.69 (SD ±4.59) years. All diagnoses were confirmed by medical record and pathology review. Information on statin use and other risk factors was collected at baseline and during follow-up. Multivariable-adjusted hazards ratios (HRs) and 95 % confidence intervals (CIs) evaluating the relationship between prior statin use (at baseline only as well as in a time-dependent manner) and risk of pancreatic cancer were computed from Cox proportional hazards regression analyses after adjusting for appropriate confounders. We also evaluated the effect of statin type, potency, lipophilic status, and duration of use. All statistical tests were two-sided. RESULTS: Statins were used at baseline by 12,243 (7.5 %) women. The annualized rate of pancreatic cancer in statin users and nonusers, respectively, was 0.0298 versus 0.0271 %. The multivariable-adjusted HR for statin users versus nonusers at baseline was 0.92 and 95 % CI 0.57-1.48. In a time-dependent model, the HR for low-potency statins was 0.46, 95 % CI 0.20-1.04. There was no significant effect seen by statin lipophilicity or duration of use. CONCLUSIONS: There was no significant relationship between statins and pancreatic cancer risk in the WHI; however, there was a marginal inverse association noted for low-potency statins. Analyses of larger numbers of cases are needed to further explore this relationship.

8 Article Intake of fruits and vegetables and risk of pancreatic cancer in a pooled analysis of 14 cohort studies. 2012

Koushik, Anita / Spiegelman, Donna / Albanes, Demetrius / Anderson, Kristin E / Bernstein, Leslie / van den Brandt, Piet A / Bergkvist, Leif / English, Dallas R / Freudenheim, Jo L / Fuchs, Charles S / Genkinger, Jeanine M / Giles, Graham G / Goldbohm, R Alexandra / Horn-Ross, Pamela L / Männistö, Satu / McCullough, Marjorie L / Millen, Amy E / Miller, Anthony B / Robien, Kim / Rohan, Thomas E / Schatzkin, Arthur / Shikany, James M / Stolzenberg-Solomon, Rachael Z / Willett, Walter C / Wolk, Alicja / Ziegler, Regina G / Smith-Warner, Stephanie A. ·University of Montreal Hospital Research Centre (CRCHUM), Montreal, Quebec, Canada. anita.koushik@umontreal.ca ·Am J Epidemiol · Pubmed #22875754.

ABSTRACT: Fruit and vegetable intake may protect against pancreatic cancer, since fruits and vegetables are rich in potentially cancer-preventive nutrients. Most case-control studies have found inverse associations between fruit and vegetable intake and pancreatic cancer risk, although bias due to reporting error cannot be ruled out. In most prospective studies, inverse associations have been weaker and imprecise because of small numbers of cases. The authors examined fruit and vegetable intake in relation to pancreatic cancer risk in a pooled analysis of 14 prospective studies from North America, Europe, and Australia (study periods between 1980 and 2005). Relative risks and 2-sided 95% confidence intervals were estimated separately for the 14 studies using the Cox proportional hazards model and were then pooled using a random-effects model. Of 862,584 men and women followed for 7-20 years, 2,212 developed pancreatic cancer. The pooled multivariate relative risks of pancreatic cancer per 100-g/day increase in intake were 1.01 (95% confidence interval (CI): 0.99, 1.03) for total fruits and vegetables, 1.01 (95% CI: 0.99, 1.03) for total fruits, and 1.02 (95% CI: 0.99, 1.06) for total vegetables. Associations were similar for men and women separately and across studies. These results suggest that fruit and vegetable intake during adulthood is not associated with a reduced pancreatic cancer risk.

9 Article Coffee, tea, and sugar-sweetened carbonated soft drink intake and pancreatic cancer risk: a pooled analysis of 14 cohort studies. 2012

Genkinger, Jeanine M / Li, Ruifeng / Spiegelman, Donna / Anderson, Kristin E / Albanes, Demetrius / Bergkvist, Leif / Bernstein, Leslie / Black, Amanda / van den Brandt, Piet A / English, Dallas R / Freudenheim, Jo L / Fuchs, Charles S / Giles, Graham G / Giovannucci, Edward / Goldbohm, R Alexandra / Horn-Ross, Pamela L / Jacobs, Eric J / Koushik, Anita / Männistö, Satu / Marshall, James R / Miller, Anthony B / Patel, Alpa V / Robien, Kim / Rohan, Thomas E / Schairer, Catherine / Stolzenberg-Solomon, Rachael / Wolk, Alicja / Ziegler, Regina G / Smith-Warner, Stephanie A. ·Mailman School of Public Health, 722 w 168th St, Rm 803, New York, NY 10032, USA. jg3081@columbia.edu ·Cancer Epidemiol Biomarkers Prev · Pubmed #22194529.

ABSTRACT: BACKGROUND: Coffee has been hypothesized to have pro- and anticarcinogenic properties, whereas tea may contain anticarcinogenic compounds. Studies assessing coffee intake and pancreatic cancer risk have yielded mixed results, whereas findings for tea intake have mostly been null. Sugar-sweetened carbonated soft drink (SSB) intake has been associated with higher circulating levels of insulin, which may promote carcinogenesis. Few prospective studies have examined SSB intake and pancreatic cancer risk; results have been heterogeneous. METHODS: In this pooled analysis from 14 prospective cohort studies, 2,185 incident pancreatic cancer cases were identified among 853,894 individuals during follow-up. Multivariate (MV) study-specific relative risks (RR) and 95% confidence intervals (CI) were calculated using Cox proportional hazards models and then pooled using a random-effects model. RESULTS: No statistically significant associations were observed between pancreatic cancer risk and intake of coffee (MVRR = 1.10; 95% CI, 0.81-1.48 comparing ≥900 to <0 g/d; 237g ≈ 8oz), tea (MVRR = 0.96; 95% CI, 0.78-1.16 comparing ≥400 to 0 g/d; 237g ≈ 8oz), or SSB (MVRR = 1.19; 95% CI, 0.98-1.46 comparing ≥250 to 0 g/d; 355g ≈ 12oz; P value, test for between-studies heterogeneity > 0.05). These associations were consistent across levels of sex, smoking status, and body mass index. When modeled as a continuous variable, a positive association was evident for SSB (MVRR = 1.06; 95% CI, 1.02-1.12). CONCLUSION AND IMPACT: Overall, no associations were observed for intakes of coffee or tea during adulthood and pancreatic cancer risk. Although we were only able to examine modest intake of SSB, there was a suggestive, modest positive association for risk of pancreatic cancer for intakes of SSB.

10 Article A pooled analysis of 14 cohort studies of anthropometric factors and pancreatic cancer risk. 2011

Genkinger, Jeanine M / Spiegelman, Donna / Anderson, Kristin E / Bernstein, Leslie / van den Brandt, Piet A / Calle, Eugenia E / English, Dallas R / Folsom, Aaron R / Freudenheim, Jo L / Fuchs, Charles S / Giles, Graham G / Giovannucci, Edward / Horn-Ross, Pamela L / Larsson, Susanna C / Leitzmann, Michael / Männistö, Satu / Marshall, James R / Miller, Anthony B / Patel, Alpa V / Rohan, Thomas E / Stolzenberg-Solomon, Rachael Z / Verhage, Bas A J / Virtamo, Jarmo / Willcox, Bradley J / Wolk, Alicja / Ziegler, Regina G / Smith-Warner, Stephanie A. ·Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY 10032, USA. jg3081@columbia.edu ·Int J Cancer · Pubmed #21105029.

ABSTRACT: Epidemiologic studies of pancreatic cancer risk have reported null or nonsignificant positive associations for obesity, while associations for height have been null. Waist and hip circumference have been evaluated infrequently. A pooled analysis of 14 cohort studies on 846,340 individuals was conducted; 2,135 individuals were diagnosed with pancreatic cancer during follow-up. Study-specific relative risks (RRs) and 95% confidence intervals (CIs) were calculated by Cox proportional hazards models, and then pooled using a random effects model. Compared to individuals with a body mass index (BMI) at baseline between 21-22.9 kg/m(2) , pancreatic cancer risk was 47% higher (95%CI:23-75%) among obese (BMI ≥ 30 kg/m(2) ) individuals. A positive association was observed for BMI in early adulthood (pooled multivariate [MV]RR = 1.30, 95%CI = 1.09-1.56 comparing BMI ≥ 25 kg/m(2) to a BMI between 21 and 22.9 kg/m(2) ). Compared to individuals who were not overweight in early adulthood (BMI < 25 kg/m(2) ) and not obese at baseline (BMI < 30 kg/m(2) ), pancreatic cancer risk was 54% higher (95%CI = 24-93%) for those who were overweight in early adulthood and obese at baseline. We observed a 40% higher risk among individuals who had gained BMI ≥ 10 kg/m(2) between BMI at baseline and younger ages compared to individuals whose BMI remained stable. Results were either similar or slightly stronger among never smokers. A positive association was observed between waist to hip ratio (WHR) and pancreatic cancer risk (pooled MVRR = 1.35 comparing the highest versus lowest quartile, 95%CI = 1.03-1.78). BMI and WHR were positively associated with pancreatic cancer risk. Maintaining normal body weight may offer a feasible approach to reducing morbidity and mortality from pancreatic cancer.

11 Article Anthropometric measures, body mass index, and pancreatic cancer: a pooled analysis from the Pancreatic Cancer Cohort Consortium (PanScan). 2010

Arslan, Alan A / Helzlsouer, Kathy J / Kooperberg, Charles / Shu, Xiao-Ou / Steplowski, Emily / Bueno-de-Mesquita, H Bas / Fuchs, Charles S / Gross, Myron D / Jacobs, Eric J / Lacroix, Andrea Z / Petersen, Gloria M / Stolzenberg-Solomon, Rachael Z / Zheng, Wei / Albanes, Demetrius / Amundadottir, Laufey / Bamlet, William R / Barricarte, Aurelio / Bingham, Sheila A / Boeing, Heiner / Boutron-Ruault, Marie-Christine / Buring, Julie E / Chanock, Stephen J / Clipp, Sandra / Gaziano, J Michael / Giovannucci, Edward L / Hankinson, Susan E / Hartge, Patricia / Hoover, Robert N / Hunter, David J / Hutchinson, Amy / Jacobs, Kevin B / Kraft, Peter / Lynch, Shannon M / Manjer, Jonas / Manson, Joann E / McTiernan, Anne / McWilliams, Robert R / Mendelsohn, Julie B / Michaud, Dominique S / Palli, Domenico / Rohan, Thomas E / Slimani, Nadia / Thomas, Gilles / Tjønneland, Anne / Tobias, Geoffrey S / Trichopoulos, Dimitrios / Virtamo, Jarmo / Wolpin, Brian M / Yu, Kai / Zeleniuch-Jacquotte, Anne / Patel, Alpa V / Anonymous3240660. ·Department of Obstetrics and Gynecology, New York University School of Medicine, 550 First Ave, TH-528, New York, NY 10016, USA. alan.arslan@nyumc.org ·Arch Intern Med · Pubmed #20458087.

ABSTRACT: BACKGROUND: Obesity has been proposed as a risk factor for pancreatic cancer. METHODS: Pooled data were analyzed from the National Cancer Institute Pancreatic Cancer Cohort Consortium (PanScan) to study the association between prediagnostic anthropometric measures and risk of pancreatic cancer. PanScan applied a nested case-control study design and included 2170 cases and 2209 control subjects. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression for cohort-specific quartiles of body mass index (BMI [calculated as weight in kilograms divided by height in meters squared]), weight, height, waist circumference, and waist to hip ratio as well as conventional BMI categories (underweight, <18.5; normal weight, 18.5-24.9; overweight, 25.0-29.9; obese, 30.0-34.9; and severely obese, > or = 35.0). Models were adjusted for potential confounders. RESULTS: In all of the participants, a positive association between increasing BMI and risk of pancreatic cancer was observed (adjusted OR for the highest vs lowest BMI quartile, 1.33; 95% CI, 1.12-1.58; P(trend) < .001). In men, the adjusted OR for pancreatic cancer for the highest vs lowest quartile of BMI was 1.33 (95% CI, 1.04-1.69; P(trend) < .03), and in women it was 1.34 (95% CI, 1.05-1.70; P(trend) = .01). Increased waist to hip ratio was associated with increased risk of pancreatic cancer in women (adjusted OR for the highest vs lowest quartile, 1.87; 95% CI, 1.31-2.69; P(trend) = .003) but less so in men. CONCLUSIONS: These findings provide strong support for a positive association between BMI and pancreatic cancer risk. In addition, centralized fat distribution may increase pancreatic cancer risk, especially in women.