Genetic polymorphism of N-acetyltransferases, glutathione S-transferase M1 and NAD(P)H: quinone oxidoreductase in relation to malignant and benign pancreatic disease risk

摘要: Carcinogens present in cigarette smoke and diet have been associated with pancreatic cancer. We hypothesized that heterocyclic aromatic amines implicated these exposures could be involved as causative agents therefore genetic variation enzymes metabolizing carcinogens modify the risk of developing malignant benign disease. The effect polymorphism acetyltransferases (NAT1) NAT2), glutathione S-transferase M1 (GSTM1) NAD(P)H: quinone oxidoreductase 1 (NQO1) on diseases (cancer, pancreatitis) was examined a case-control study. PCR-based assays were used for genotype analysis genomic DNA from whole blood cells. Samples collected Caucasian patients diagnosed cancer (n = 81), non-alcoholic 41) alcoholic pancreatitis 73) asymptomatic control subjects 78) analysed. prevalence GSTM1 null NAT2 fast slow acetylator genotypes distribution frequencies NQO1 did not differ vs controls. For NAT1 acetylators non-significant excess (P 0.18) found among cases There significant over-representation AB or B all disease combined (OR 2.6; P < 0.05). When concurrent controls pooled literature 1427), OR 1.4 0.08). results this study, requiring confirmation, suggest may modest increase susceptibility to diseases.