N-Acetyltransferase-2, glutathione S-transferase M1 and T1 genetic polymorphisms, cigarette smoking and hepatocellular carcinoma: A case-control study

✍ Scribed by Umberto Gelatti; Loredana Covolo; Renato Talamini; Alessandro Tagger; Fabio Barbone; Claudia Martelli; Francesca Cremaschini; Silvia Franceschi; Maria Lisa Ribero; Seymour Garte; Giuseppe Nardi; Valter Donadon; Francesco Donato

• Publisher: John Wiley and Sons
• Year: 2005
• Tongue: French
• Weight: 93 KB
• Volume: 115
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.20895

✦ Synopsis

Abstract

Our aim was to evaluate the role of N‐acetyltransferase (NAT2) and glutathione S‐transferase M1 and T1 (GSTM1 and GSTT1) polymorphisms in hepatocellular carcinoma (HCC) according to cigarette smoking, taking into account hepatitis B (HBV) and C (HCV) viral infection as well as alcohol consumption. A hospital‐based case‐control study was conducted in 2 areas of north Italy. Cases (n = 200) were patients hospitalized for HCC, and controls (n = 400) were patients admitted for reasons other than liver disease, neoplasms and tobacco‐ and alcohol‐related diseases. Genotypes were determined using PCR and the PCR/restriction fragment length polymorphism–based method. The putative risk genotypes NAT2 slow acetylator, GSTM1 null and GSTT1 null were not associated with HCC (OR = 1.3, 95% CI 0.8–2.0; OR = 1.0, 95% CI 0.6–1.5; OR = 0.8, 95% CI 0.4–1.4, respectively). Although not statistically significant, an increase in HCC risk was observed among light smokers (1–20 pack‐years) carrying GSTT1 null (OR = 1.7, 95% CI 0.6–4.7) and NAT2 slow acetylator (OR = 1.3, 95% CI 0.6–3.0) genotypes. In conclusion, there was no evidence for a gene–environment interaction in HCC risk for GSTM1, GSTT1 and NAT2 genotypes. © 2005 Wiley‐Liss, Inc.