© 2001 by Oxford University Press
Journal of the National Cancer Institute, Vol. 93, No. 12, 937-941,
June 20, 2001
© 2001 Oxford University Press
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Helicobacter pylori Seropositivity as a Risk Factor for Pancreatic Cancer
Affiliations of authors: R. Z. Stolzenberg-Solomon (Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics and Cancer Prevention Studies Branch, Division of Clinical Sciences), P. J. Limburg, P. R. Taylor (Cancer Prevention Studies Branch, Division of Clinical Sciences), D. Albanes (Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics), National Cancer Institute, Bethesda, MD; M. J. Blaser, Departments of Medicine and Microbiology, New York University School of Medicine and Department of Veterans Affairs Medical Center, New York; G. Perez-Perez, Departments of Medicine and Microbiology, New York University School of Medicine; J. Virtamo, National Public Health Institute, Helsinki, Finland.
Correspondence to: Rachael Z. Stolzenberg-Solomon, Ph.D., M.P.H., National Institutes of Health, 6120 Executive Blvd., MSC 7026, Rm. 7039, Bethesda, MD 20892 (e-mail: rs221z{at}nih.gov).
Background: Pancreatic cancer is among the most fatal cancers worldwide and one for which few preventable risk factors have been established. Gastric carriage of Helicobacter pylori, particularly cytotoxin-associated gene-A-positive (CagA+) strains, is known to be a risk factor for peptic ulcer disease and gastric cancer and may have a similar etiologic relationship with pancreatic cancer. Methods: We investigated the association of H. pylori carriage and exocrine pancreatic cancer in 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 at baseline. Case subjects (n = 121) were matched on date of baseline serum collection, study center, age, trial intervention, and completion of the dietary questionnaire to 226 control subjects who were alive at the time the matching case subject was diagnosed and who remained free of cancer, during up to 10 years of follow-up. Levels of immunoglobulin G antibodies to H. pylori whole-cell and CagA+ antigens from stored baseline serum were measured by enzyme-linked immunosorbent assay. Smoking-adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by use of conditional logistic regression. Statistical tests were two-sided. Results: Seroprevalence of H. pylori was 82% and 73% among case and control subjects, respectively. Compared with seronegative subjects, those with H. pylori or CagA+ strains were at statistically significantly elevated risk of pancreatic cancer (OR = 1.87 [95% CI = 1.05 to 3.34]; OR = 2.01 [95% CI = 1.09 to 3.70], respectively). Conclusions: Our findings support a possible role for H. pylori carriage in the development of exocrine pancreatic cancer.
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