Abstract
Objective:Our aim was to evaluate whether the association of GSTM1/T1 gene polymorphisms modifies the risk of Hepatocellular carcinoma (HCC) and what is its correlation with other predisposing risk factors like alcohol intake, cigarette smoking and hepatitis B and C infections.Study design/setting:It was a case-control study, included 254 HCC cases compared with 525 hospital-based age and sex matched cases of chronic liver disease without HCC as controls from Indian population. The GSTM1 and GSTT1 genotypes were detected using conventional multiplex PCR method.Results:In this case-control study, we observed a positive correlation between age, HBV and HCV infection, smoking habit of > 20 packs/year, alcohol consumption of > 100 g/day and risk of liver cancer. We found significantly increased risk associated with GSTM1 null genotype (OR = 3.49; 95% CI = 2.52–4.84) as well as GSTT1 null genotype (OR = 3.12; 95% CI = 2.19–4.45), respectively. However, an increased risk of HCC was observed among heavy drinkers with GSTM1 (OR = 2.01; 95% CI = 1.11–3.66). Further, cigarette smoking showed a non-significant association with GSTT1 (OR = 1.49; CI = 0.69–3.25).Conclusion:Our results suggest that the variants in low penetrance gene such as GSTM1 and GSTT1 are associated with an increased liver cancer risk. Further, an influence of GSTM1/T1 null genotypes may contribute in the etiology of HCC in patients with higher cigarette and alcohol consumption.
Highlights
Hepatocellular carcinoma (HCC) is one of the most commonly occurring solid tumors worldwide, and is the most frequent cause of cancer-related death in subSaharan Africa and China, among other regions
Both HBV surface antigen (HBsAg) and hepatitis C virus (HCV) RNA positivity were associated with HCC
HCV positivity poses a two fold increased risk with HCC (OR = 2.2; 95% CI = 1.34–3.61; Table 1)
Summary
Hepatocellular carcinoma (HCC) is one of the most commonly occurring solid tumors worldwide, and is the most frequent cause of cancer-related death in subSaharan Africa and China, among other regions. Moyer et al suggested that functionally significant pharmacogenomic variations, such as single nucleotide polymorphisms (SNP), might be sufficient to contribute either to carcinogenesis or to individual variations in antineoplastic drug therapy response [16] Carcinogens such as aflatoxin B1-8, 9-epoxide are a substrate for both GSTM1 and GSTT1 [15]. One study found no association between HCC and GSTM1/T1 gene deletion in smokers [8], another found a non significantly increased risk of HCC among light smokers (1–20 pack-years) carrying GSTT1-null and NAT2-slow-acetylator genotypes [27]. Types and the risk of developing HCC, taking into account the smoking habits, HBV and HCV infection status, and alcohol consumption in subjects in two Indian populations
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