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  • 1
    Publication Date: 2018-03-06
    Description: Background: Nut intake has been associated with decreased cancer-related mortality, but few studies have examined the potential of nuts in the chemoprevention of pancreatic cancer. We prospectively investigated the association of total nut, tree nut, peanut, and peanut butter consumption with pancreatic cancer risk. Methods: In the Netherlands Cohort Study, 120,852 men and women completed a baseline questionnaire, including a food frequency questionnaire, in 1986. After 20.3 years of follow-up, 583 incident pancreatic cancer cases, including 349 microscopically confirmed pancreatic cancer (MCPC) cases, were included in multivariable case–cohort analyses. Results: Increased total nut consumption was associated with a nonsignificantly decreased MCPC risk in men [HR (95% confidence interval) for 10+ g/d vs. nonconsumers = 0.72 (0.47–1.11), P trend = 0.163]. No clear association was found in women. For tree nut and peanut consumption, nonsignificant inverse associations were observed in men. In women, no or unclear associations were found for tree nut and peanut consumption. Peanut butter intake was related to a significantly reduced risk of MCPC in men [HR (95% confidence interval) for 5+ g/d vs. nonconsumers = 0.53 (0.28–1.00), P trend = 0.047], but this relation was not clear in women. Evidence for a nonlinear dose–response relation with MCPC was found for tree nut intake only. The associations were weaker when looking at total pancreatic cancer. Conclusions: Our results suggest that nuts and peanut butter might reduce pancreatic cancer risk in men. In women, no or unclear associations were found. Impact: Nut consumption might reduce the risk of pancreatic cancer in men. Cancer Epidemiol Biomarkers Prev; 27(3); 274–84. ©2018 AACR .
    Print ISSN: 1055-9965
    Electronic ISSN: 1538-7755
    Topics: Medicine
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  • 2
    Publication Date: 2018-03-09
    Description: The alcohol–colorectal cancer (CRC) association may differ by sex and ADH1B and ADH1C genotypes. ADH enzymes oxidize ethanol to acetaldehyde, both of which are human carcinogens. The Netherlands Cohort Study includes 120 852 participants, aged 55–69 years at baseline (1986), and has 20.3 years follow-up (case-cohort: n subcohort = 4774; n cases = 4597). The baseline questionnaire included questions on alcohol intake at baseline and 5 years before. Using toenail DNA, available for ~75% of the cohort, we successfully genotyped six ADH1B and six ADH1C SNPs ( n subcohort = 3897; n cases = 3558). Sex- and subsite-specific Cox hazard ratios and 95% confidence intervals for CRC were estimated comparing alcohol categories, genotypes within drinkers and alcohol categories within genotype strata. We used a dominant genetic model and adjusted for multiple testing. Alcohol intake increased CRC risk in both sexes, though in women only in the (proximal) colon when in excess of 30 g/day. In male drinkers, ADH1B rs4147536 increased (distal) colon cancer risk. In female drinkers, ADH1C rs283415 increased proximal colon cancer risk. ADH1B rs3811802 and ADH1C rs4147542 decreased CRC risk in heavy (〉30 g/day) and stable drinkers (compared to 5 years before baseline), respectively. Rs3811802 and rs4147542 significantly modified the alcohol-colon cancer association in women ( P for interaction = 0.004 and 0.02, respectively). A difference in associations between genotype strata was generally clearer in men than women. In conclusion, men showed increased CRC risks across subsites and alcohol intake levels, while only colon cancer risk was increased in women at heavy intake levels. ADH1B rs3811802 and ADH1C rs4147542 significantly modified the alcohol–colon cancer association in women.
    Print ISSN: 0143-3334
    Electronic ISSN: 1460-2180
    Topics: Medicine
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