title: Helicobacter pylori seropositivity as a risk factor for pancreatic cancer.
abstract: 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.
authors: Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics and Cancer Prevention Studies Branch, Division of Clinical Sciences, National Cancer Institute, Bethesda, MD 20892, USA. rs221z@nih.gov
authors: R Z
authors: RZ
authors: Stolzenberg-Solomon
authors: M J
authors: MJ
authors: Blaser
authors: P J
authors: PJ
authors: Limburg
authors: G
authors: G
authors: Perez-Perez
authors: P R
authors: PR
authors: Taylor
authors: J
authors: J
authors: Virtamo
authors: D
authors: D
authors: Albanes
mesh_terms: D000368:Aged; D000428:Alcohol Drinking; D000907:Antibodies, Bacterial / Q000097:blood*; D016588:Anticarcinogenic Agents / Q000627:therapeutic use; D003069:Coffee; D015331:Cohort Studies; D004311:Double-Blind Method; D002149:Energy Intake; D005387:Finland / Q000453:epidemiology; D005500:Follow-Up Studies; D016480:Helicobacter pylori / Q000276:immunology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009369:Neoplasms / Q000453:epidemiology / Q000209:etiology / Q000517:prevention & control*; D010190:Pancreatic Neoplasms / Q000453:epidemiology* / Q000382:microbiology; D012016:Reference Values; D012307:Risk Factors; D012907:Smoking; D013997:Time Factors; D014810:Vitamin E / Q000627:therapeutic use; D019207:beta Carotene / Q000627:therapeutic use
chemical_list: D000907:Antibodies, Bacterial; D016588:Anticarcinogenic Agents; D003069:Coffee; D019207:beta Carotene; D014810:Vitamin E