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N‐Acetyltransferase‐2, glutathione S‐transferase M1 and T1 genetic polymorphisms, cigarette smoking and hepatocellular carcinoma: A case‐control study
Author(s) -
Gelatti Umberto,
Covolo Loredana,
Talamini Renato,
Tagger Alessandro,
Barbone Fabio,
Martelli Claudia,
Cremaschini Francesca,
Franceschi Silvia,
Ribero Maria Lisa,
Garte Seymour,
Nardi Giuseppe,
Donadon Valter,
Donato Francesco
Publication year - 2005
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.20895
Subject(s) - genotype , gstp1 , hepatocellular carcinoma , glutathione s transferase , medicine , gastroenterology , case control study , alcohol consumption , glutathione , biology , alcohol , gene , genetics , enzyme , biochemistry
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.