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

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

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1
Toxicogenomics Unit, National Institute of Public Health, Prague, Czech Republic.

Abstract

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.

PMID:
19812523
DOI:
10.1097/MPA.0b013e3181bab6c2
[Indexed for MEDLINE]
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