Results
PMID | 26370772 |
Gene Name | GSTT1 |
Condition | Endometriosis |
Association |
Associated |
Population size | 917 |
Population details | 917 (404 cases, 513 controls) |
Sex | Female |
Other associated phenotypes |
Endometriosis |
Gynecol Endocrinol. 2015;31(11):840-5. doi: 10.3109/09513590.2015.1080681. Epub Chen, Xin-Ping| Xu, Da-Feng| Xu, Wei-Hua| Yao, Jia| Fu, Sheng-Miao a Department of Central Laboratory , Hainan Province People's Hospital , Haikou, Hainan Province , China .| b College of Agriculture, Hainan University , Haikou, Hainan Province , China .| c Department of Hepatobiliary Surgery , Hainan Province People In view of the controversies surrounding the glutathione-S-transferases (GST) M1/T1-endometriosis association, a meta-analysis of the GSTM1/GSTT1 genetic association studies of endometriosis was performed in Chinese populations. PubMed, Springer Link, OvidSP, and Chinese databases were searched for related studies. A total of nine studies on GSTM1-endometriosis involved 874 cases and 997 controls, and five studies on GSTT1 involved 404 cases and 513 controls were included in this meta-analysis. Overall, the null genotype of GSTM1/GSTT1 was significantly related to endometriosis risk in Chinese populations (GSTM1, OR = 2.21, 95% CI: 1.22-4.01; GSTT1, OR = 2.31, 95% CI: 1.34-3.99). In subgroup analyses stratified by ethnicity and source of controls, the same results were observed in Chinese Han and population-based studies. The sensitivity analysis confirmed the reliability and stability of the meta-analysis. No publication bias was found among studies by Egger's test. In conclusion, our meta-analysis supports that the GSTM1/GSTT1 null genotype might contribute to individual susceptibility to endometriosis in Chinese populations, especially in Chinese Han. Mesh Terms: Asian Continental Ancestry Group/*genetics| China| Endometriosis/*genetics| Female| Genetic Predisposition to Disease| Genotype| Glutathione Transferase/*genetics| Humans| Polymorphism, Genetic| Polymorphism, Single Nucleotide|DA 2016/09/13 06:00 |