BACKGROUND & AIMS: Studies investigating the associations between glutathione S-transferase (GST) genetic polymorphisms and hepatocellular carcinoma (HCC) risk have reported controversial results. Thus, a meta-analysis was performed to clarify the effects of GSTM1 and GSTT1 polymorphisms on HCC risk. METHODS: We identified 132 relevant records through a literature search up to November 22, 2009, and 24 individual case-control studies from 23 publications were finally included, involving a total of 3349 HCC cases and 5609 controls. Subgroup analyses were performed by ethnicity, or by area according to the incidence rate and hepatitis virus status. RESULTS: Analyses of total relevant studies showed an increased HCC risk was significantly associated with null genotypes of GSTM1 (OR=1.26, 95% CI 1.03-1.54, p(OR)=0.027) and GSTT1 (OR=1.28, 95% CI 1.09-1.51, p(OR)=0.002). In addition, the GSTM1-GSTT1 interaction analysis showed that the dual null genotype of GSTM1/GSTT1 was significantly associated with increased HCC risk (OR=1.89, 95% CI 1.38-2.60, p(OR)<0.001). Subgroup analyses showed that the associations above were still statistically significant in Asians (p(GSTM1)=0.017, p(GSTT1)=0.001, p(Dual null genotype)<0.001), high-rate areas (p(GSTM1)=0.012, p(GSTT1)=0.006, p(Dual null genotype)<0.001), and HBV-dominant areas (p(GSTM1)=0.003, p(GSTT 1)=0.003, p(Dual null genotype)<0.001). CONCLUSIONS: This meta-analysis suggests null genotypes of GSTM1 and GSTT1 are both associated with increased HCC risk in Asians, and individuals with the dual null genotype of GSTM1/GSTT1 are particularly susceptible to developing HCC. Copyright 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
BACKGROUND & AIMS: Studies investigating the associations between glutathione S-transferase (GST) genetic polymorphisms and hepatocellular carcinoma (HCC) risk have reported controversial results. Thus, a meta-analysis was performed to clarify the effects of GSTM1 and GSTT1 polymorphisms on HCC risk. METHODS: We identified 132 relevant records through a literature search up to November 22, 2009, and 24 individual case-control studies from 23 publications were finally included, involving a total of 3349 HCC cases and 5609 controls. Subgroup analyses were performed by ethnicity, or by area according to the incidence rate and hepatitis virus status. RESULTS: Analyses of total relevant studies showed an increased HCC risk was significantly associated with null genotypes of GSTM1 (OR=1.26, 95% CI 1.03-1.54, p(OR)=0.027) and GSTT1 (OR=1.28, 95% CI 1.09-1.51, p(OR)=0.002). In addition, the GSTM1-GSTT1 interaction analysis showed that the dual null genotype of GSTM1/GSTT1 was significantly associated with increased HCC risk (OR=1.89, 95% CI 1.38-2.60, p(OR)<0.001). Subgroup analyses showed that the associations above were still statistically significant in Asians (p(GSTM1)=0.017, p(GSTT1)=0.001, p(Dual null genotype)<0.001), high-rate areas (p(GSTM1)=0.012, p(GSTT1)=0.006, p(Dual null genotype)<0.001), and HBV-dominant areas (p(GSTM1)=0.003, p(GSTT 1)=0.003, p(Dual null genotype)<0.001). CONCLUSIONS: This meta-analysis suggests null genotypes of GSTM1 and GSTT1 are both associated with increased HCC risk in Asians, and individuals with the dual null genotype of GSTM1/GSTT1 are particularly susceptible to developing HCC. Copyright 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.
Authors: Michael O Baclig; May R Alvarez; Xerxes Morgan R Lozada; Cynthia A Mapua; Jingky P Lozano-Kühne; Mark Pierre S Dimamay; Filipinas F Natividad; Juliet Gopez-Cervantes; Ronald R Matias Journal: Int J Mol Epidemiol Genet Date: 2012-05-15
Authors: Patricia A Egner; Jian Guo Chen; Jin Bing Wang; Yan Wu; Yan Sun; Jian Hua Lu; Jian Zhu; Yong Hui Zhang; Yong Sheng Chen; Marlin D Friesen; Lisa P Jacobson; Alvaro Muñoz; Derek Ng; Geng Sun Qian; Yuan Rong Zhu; Tao Yang Chen; Nigel P Botting; Qingzhi Zhang; Jed W Fahey; Paul Talalay; John D Groopman; Thomas W Kensler Journal: Cancer Prev Res (Phila) Date: 2011-03