GSTM1 null allele is a risk factor for gastric cancer development in Asians.
ABSTRACT Glutathione S-transferase M1 (GSTM1), which plays an important role in detoxification pathways to protect against damage caused by reactive metabolites of chemicals, has been considered as potential gastric cancer susceptibility genes. However, the published data on the association between GSTM1 present/null polymorphism and gastric cancer risk are still inconclusive. To derive a more precise estimation of the relationship, a meta-analysis was performed. Totally, 44 studies including 5440 cases and 11607 controls were involved in the analysis. When all studies were pooled into the meta-analysis, obviously increased gastric cancer risk was found in null genotype carriers (OR=1.19, 95% CI: 1.08-1.33). When stratified by ethnicity, obviously evaluated risk was found in Asians (OR=1.31, 95% CI: 1.11-1.54) but not reached to statistically significance in Caucasians (OR=1.11, 95% CI: 0.96-1.28). In the subgroup analysis by hospital-based studies or population-based studies, statistically significantly elevated risk was found in hospital-based studies (OR=1.34, 95% CI: 1.07-1.67) but not reached to statistically significance in population-based studies (OR=1.11, 95% CI: 0.99-1.25). In summary, this meta-analysis result indicates that the GSTM1 null genotype is a low-penetrant risk factor for gastric cancer development in Asians.
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ABSTRACT: Glutathione S-transferases M1 (GSTM1) is an important phase II metabolizing enzyme. The null genotype of GSTM1 causes total loss of GSTM1 enzyme activity and numerous studies have investigated the association between GSTM1 null genotype and gastric cancer risk. This meta-analysis was designed to investigate the relationship between GSTM1 null genotype and susceptibility to gastric cancer and assess the influence of Helicobacter pylori infection, smoking, Lauren's classification, and other factors. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to estimate the association strength. A total of 46 eligible studies were indentified and analyzed in this meta-analysis, including 8138 cases of gastric cancer and 13867 controls. Pooled results showed that the GSTM1 null genotype was associated with a significantly increased risk of gastric cancer (OR=1.217, 95% CI: 1.113-1.331, Pheterogeneity<0.001). Sub-group analysis suggested that the significant association was only observed in Asians (OR=1.273, 95%: 1.137-1.426, Pheterogeneity = 0.002), but not in Caucasians. The increased risk was found among H. pylori positive population (OR=1.928, 95% CI: 1.028-3.615, Pheterogeneity=0.065), while no association was found among H. pylori negative population (OR=0.969, 95% CI: 0.618-1.521, Pheterogeneity=0.168). For smoking status, the GSTM1 null genotype increased risk of gastric cancer in both ever-smokers and non-smokers. Source of control, sample size, location of tumor and Lauren's classification did not modify the association. In this meta-analysis based on 46 epidemiological studies, we show that the GSTM1 null genotype is associated with an increased risk of gastric cancer among Asians but not among Caucasians. H. pylori infection but not smoking status could modify the association.PLoS ONE 01/2013; 8(11):e81403. · 3.53 Impact Factor
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ABSTRACT: Previous studies have suggested that the glutathione S-transferases M1 (GSTM1) null genotype is associated with the risk of gastric cancer. However, the interaction between GSTM1 null genotype and smoking for the risk of gastric cancer is still elusive. Therefore, we performed a meta-analysis to ascertain this issue. Databases of PubMed, EMBASE, and China National Knowledge Infrastructure were searched to retrieve relevant studies. Smokers were categorized as "ever-smokers" and "non-smokers." Odds ratios (ORs) and 95 % confidence intervals (95 % CIs) were calculated to estimate the association strength. Subgroup analyses according to ethnicity, source of control, and sample size were also conducted. A total of 15 eligible studies, including 4,687 gastric cancer cases and 7,002 controls, were identified. We found that the GSTM1 null genotype was associated with increased risk of gastric cancer among ever-smokers (OR = 1.460, 95 % CI 1.064-2.003, heterogeneity: P = 0.019). The null genotype also significantly increased the risk of gastric cancer among non-smokers (OR = 1.777, 95 % CI 1.301-2.426, heterogeneity: P < 0.01). Stratified analysis according to ethnicity showed that the GSTM1 null genotype was associated with increased risk of gastric cancer among Asians both in ever-smokers (OR = 1.841, 95 % CI 1.184-2.861) and non-smokers (OR = 1.773, 95 % CI 1.382-2.275). In conclusion, the GSMT1 null genotype significantly increased the risk of gastric cancer both in ever-smokers and non-smokers.Tumor Biology 12/2013; · 2.52 Impact Factor
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ABSTRACT: The Glutathione S-transferase M1 (GSTM1) and Glutathione S-transferase T1 (GSTT1) genes have been studied extensively as potential candidate genes for the risk of Parkinson's disease (PD). However, direct evidence from genetic association studies remains inconclusive. In order to address this issue, we performed an updated and refined meta-analysis to determine the effect of GSTM1 and GSTT1 polymorphisms on Parkinson's disease. A fixed-effect model was utilized to calculate the combined odds ratio (OR), OR of different ethnicities, and 95% confidence intervals (CIs). Potential publication bias was estimated. Homogeneity of the included studies was also evaluated. The pooled OR was 1.13 [95% CI (1.03, 1.24)] and 0.96 [95% CI (0.82, 1.12)] for GSTM1 and GSTT1 polymorphisms, respectively. Analysis according to different races found no association between GSTM1/GSTT1 polymorphisms and PD risks except for GSTM1 variant in Caucasians, which showed a weak correlation (OR 1.16 [95% CI (1.04, 1.29), I squared=6.2%, p=0.384]). Neither publication bias nor heterogeneity was found among the included studies. The results of this meta-analysis suggest that GSTM1 polymorphism is weakly associated with the risk of PD in Caucasians whereas GSTT1 polymorphism is not a PD risk factor.Journal of the neurological sciences 12/2013; · 2.32 Impact Factor