Tehran University of Medical Sciences Iranian Journal of Public Health 2251-6085 45 9 2016 10 10 1103 1117 Dingyun YOU Dept. of Science and Technology, Kunming Medical University, Kunming, China Nanjia LU Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, China Donghui DUAN Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, China Hui LI Institute of Non-Communicable Disease Control and Prevention, Ningbo Municipal Center for Disease Control and Prevention, Ningbo , China Wenhua XING Zhejiang Provincial Key Laboratory of Pathophysiology, School of Medicine, Ningbo University, Ningbo, China 2016 09 27 2016 09 27 Background: Glutathione S-transferases (GSTs) have been investigated as potential carcinoma susceptible genes. However, the relationship between GSTs (GSTM1, GSTT1) variants and gastric carcinoma (GC) risk has been controversial in Chinese population. Methods: A comprehensive literature search strategy (PubMed, Chinese Biomedical Database, Chinese National Knowledge Infrastructure, Wan fang Database, etc.) was launched. Crude odds ratios (ORs) and confidence intervals (95% CI) were applied to estimate the strength of the association. Results: Significant associations between GSTs genetic polymorphisms and GC were evidenced under random-effects model (ORGSTM1=1.56, 95% CI: 1.39 to 1.76, I2=50.7%, P<0.0001; ORGSTT1=1.24, 95% CI: 1.10 to 1.39, I2=43.6%, P=0.014; ORGSTM1-GSTT1=1.51, 95% CI: 1.26 to 1.81, I2=59.7%, P=0.004). The pooled ORs were not qualitatively changed when any single study was omitted by sensitivity analysis. Conclusion: Our results indicated an increased GC risk in Chinese population with GSTM1 and GSTT1 null genotype and GSTM1-GSTT1 dual null genotype. Further multi-center studies are needed to investigate the gene-gene and gene-environment interactions on the susceptibility of GC.   https://ijph.tums.ac.ir/index.php/ijph/article/view/7846 https://ijph.tums.ac.ir/index.php/ijph/article/download/7846/5545