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The association between N‐acetyltransferase 2 gene polymorphisms and pancreatic cancer
Author(s) -
Ayaz Lokman,
Ercan Bahadır,
Dirlik Musa,
Atik Uğur,
Tamer Lülüfer
Publication year - 2008
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1445
Subject(s) - n acetyltransferase , pancreatic cancer , genotyping , arylamine n acetyltransferase , acetylation , genotype , carcinogen , gene , cancer , acetyltransferase , odds ratio , biology , pancreas , phenotype , microbiology and biotechnology , enzyme , genomic dna , genetics , chemistry , biochemistry , medicine
Pancreatic cancer has been linked with exposure to environmental chemicals, which generally require metabolic activation to highly reactive toxic or carcinogenic intermediates. N ‐ acetyltransferase 1 ( NAT1 ) and N‐acetyltransferase 2 ( NAT2 ) are expressed primarily in extrahepatic and hepatic tissues, respectively. Both enzymes catalyze N ‐ and O ‐acetylation of aromatic and heterocyclic amines. It is believed that these compounds are activated via O ‐acetylation and detoxified by N ‐acetylation. Several polymorphisms of these two genes have been associated with an increased risk of cancer. Twenty‐seven cases of pancreatic cancer and 104 controls were included in this study. Blood was collected in EDTA‐containing tubes, and genomic DNA was extracted from the white blood cells by using a high pure PCR template preparation kit. Genotyping of NAT2 polymorphisms was detected by a real time PCR instrument. There was a significant difference in the distribution of the NAT2*6A acetylators phenotype between cases and the controls. The odds ratio of pancreatic cancer for the NAT2*6A slow phenotype was 5.7 (95% CI = 1.27–25.55; p = 0.023) compared with the fast type. Our results suggest that slow acetylators have higher risk of developing pancreatic cancer than fast acetylators. NAT2 gene polymorphisms may be associated with genetic susceptibility to pancreatic cancer. Copyright © 2007 John Wiley & Sons, Ltd.