© 1999 by Oxford University Press
Journal of the National Cancer Institute, Vol. 91, No. 6, 535-541,
March 17, 1999
© 1999 Oxford University Press
REPORTS |
Pancreatic Cancer Risk and Nutrition-Related Methyl-Group Availability Indicators in Male Smokers
Affiliations of authors: R. Z. Stolzenberg-Solomon, Cancer Prevention Studies Branch, Division of Clinical Sciences, National Cancer Institute, Bethesda, MD, and Department of Epidemiology, The Johns Hopkins University School of Hygiene and Public Health, Baltimore, MD; D. Albanes, T. J. Hartman, J. A. Tangrea, P. R. Taylor, Cancer Prevention Studies Branch, Division of Clinical Sciences, National Cancer Institute; F. J. Nieto, Department of Epidemiology, The Johns Hopkins University School of Hygiene and Public Health; M. Rautalahti, J. Virtamo, National Public Health Institute, Helsinki, Finland; J. Sehlub, U.S. Department of Agriculture, Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center at Tufts University, Boston.
Correspondence to: Rachael Z. Stolzenberg-Solomon, Ph.D., M.P.H., R.D., National Institutes of Health, 6006 Executive Blvd., Suite 321, Bethesda, MD 20892-7058 (e-mail: RS221Z{at}NIH.GOV).
BACKGROUND: Few risk factors for pancreatic cancer have been identified, with age and cigarette smoking being the most consistent. The protective effect associated with consumption of fruits and vegetables—the major dietary sources of folate—is suggestive of a role for factors influencing cellular methylation reactions; however, to our knowledge, no study has investigated this relationship. Whether biochemical indicators of methyl-group availability are associated with exocrine pancreatic cancer risk was the focus of this investigation. METHODS: We conducted a nested case-control study within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort of 29 133 male Finnish smokers aged 50-69 years. One hundred twenty-six subjects with incident exocrine pancreatic cancer were matched by date of baseline blood draw (±30 days), study center, age (±5 years), trial intervention group, and completion of dietary history to 247 control subjects, who were alive and free from cancer at the time the case subjects were diagnosed. Odds ratios (ORs) and 95% confidence intervals (CIs) were determined by use of conditional logistic regression. Reported P values are two-tailed. RESULTS: Serum folate and pyridoxal-5'-phosphate (PLP) concentrations showed statistically significant inverse dose-response relationships with pancreatic cancer risk, with the highest serum tertiles having approximately half the risk of the lowest (folate: OR = 0.45; 95% CI = 0.24-0.82; P for trend = .009, and PLP: OR = 0.48; 95% CI = 0.26-0.88; P for trend = .02). An increased pancreatic cancer risk was also observed with greater exposure to cigarettes (e.g., pack-years [number of packs smoked per day x number of years of smoking], highest versus lowest quartile: OR = 2.13; 95% CI = 1.13-3.99; P for trend = .04). CONCLUSIONS: These results support the hypothesis that maintaining adequate folate and pyridoxine status may reduce the risk of pancreatic cancer and confirm the risk previously associated with cigarette smoking.
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