CYP2A13, ADH1B, and ADH1C gene polymorphisms and pancreatic cancer risk

Pancreas. 2010 Mar;39(2):144-8. doi: 10.1097/MPA.0b013e3181bab6c2.


Objectives: Pancreatic carcinoma etiology and molecular pathogenesis are weakly understood. Based on the assumption that genetic variation in carcinogen metabolism further modifies the risk of exposure-related cancers, we studied the association of polymorphisms in the tobacco carcinogen-metabolizing gene CYP2A13 (Arg101Stop) and the alcohol-metabolizing genes ADH1B (Arg48His) and ADH1C (Ile350Val) with pancreatic cancer risk.

Methods: Polymorphisms were studied by allelic discrimination.

Results: In a hospital-based case-control study, CYP2A13 variant alleles coding an inactive enzyme were found in 7 of 265 cancer-free controls and in none of 235 pancreatic carcinoma patients. Neither ADH1B or ADH1C polymorphisms alone nor their combinations showed a significant effect on pancreatic cancer risk.

Conclusions: The first study of the roles of CYP2A13, ADH1B, and ADH1C in pancreatic cancer etiology suggested that the controls may have a lower ability to bioactivate tobacco-derived procarcinogens than the cases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Alcohol Dehydrogenase / genetics*
  • Aryl Hydrocarbon Hydroxylases / genetics*
  • Carcinoma / enzymology
  • Carcinoma / genetics*
  • Case-Control Studies
  • Female
  • Gene Expression Regulation, Enzymologic
  • Gene Expression Regulation, Neoplastic
  • Gene Frequency
  • Genetic Predisposition to Disease
  • Hospitals
  • Humans
  • Logistic Models
  • Male
  • Middle Aged
  • Odds Ratio
  • Pancreatic Neoplasms / enzymology
  • Pancreatic Neoplasms / genetics*
  • Polymorphism, Genetic*
  • Risk Assessment
  • Risk Factors


  • ADH1B protein, human
  • ADH1C protein, human
  • Alcohol Dehydrogenase
  • Aryl Hydrocarbon Hydroxylases
  • CYP2A13 protein, human