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Pancreatic Neoplasms: HELP
Articles by Jo L. Freudenheim
Based on 5 articles published since 2010
(Why 5 articles?)
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Between 2010 and 2020, J. L. Freudenheim wrote the following 5 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 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.

4 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.

5 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.