Mutagenesis Advance Access originally published online on March 3, 2006
Mutagenesis 2006 21(2):115-123; doi:10.1093/mutage/gel005
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Glutathione S-transferase T1 status and gastric cancer risk: a meta-analysis of the literature
Institute of Hygiene, Catholic University of Sacred Heart, L.go F.Vito, 1-00168 Rome, Italy
To clarify the risk of gastric cancer associated with glutathione S-transferase T1 (GSTT1) status, a meta-analysis of published studies was performed. Eligible studies included all reports investigating an association between GSTT1 status and gastric cancer published before October 31, 2005. A qualitative scoring of papers was applied to evaluate the quality of the published data. The principal outcome measure was the odds ratio (OR) for the risk of gastric cancer associated with GSTT1 deletion status using a random effects model. Eighteen case–control studies detailing a possible association between the GSTT1 null genotype and gastric cancer were selected. Combining data from these studies, totalling 2508 cases and 4634 controls, a non-statistically significant OR for gastric cancer risk associated with GSTT1 deficiency emerged [OR = 1.09; 95% confidence interval (CI): 0.97–1.21; I2 = 0%]. When only high-quality scored studies were considered, a statistically significant increased risk appeared (OR = 1.23; 95% CI: 1.04–1.45; I2 = 0%), as well as considering only Caucasians (OR = 1.23; 95% CI: 1.03–1.56; I2 = 0%). By pooling data from seven studies (319 cases and 656 controls) that considered combinations of GSTT1 and GSTM1 genotypes, a statistically significant increased risk for gastric cancer (OR = 1.95, 95% CI: 1.42–2.67; I2 = 0%) was detected for individuals with deletion mutations in both genes compared with wild-types. In conclusion, this meta-analysis suggests that the GSTT1 null genotype may slightly increase the risk of gastric cancer and that interaction between unfavourable GST genotypes may exist. Greater attention should, therefore, be paid to the design of future studies; the investigation of interactions among multiple genotypes and environmental exposures are justified to clarify GSTT1 null status influence on gastric cancer risk.
* To whom correspondence should be addressed. Tel: 0039 06 35001527; Fax: 0039 06 35001522; Email: sboccia{at}rm.unicatt.it
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