Yin Xiuxiu, Chen Jie
Department of Scientific Research, Jining No. 1 People's Hospital, Jining, China.
Department of Maternal and Child Health, School of Public Health, Shandong University, Jinan 250012, China.
Int J Prev Med. 2017 Jun 23;8:47. doi: 10.4103/ijpvm.IJPVM_346_15. eCollection 2017.
Epidemiological evidence on the association between genetic polymorphisms in glutathione S-transferases M1 (GSTM1) and T1 (GSTT1) genes and risk of endometrial cancer (EC) has been inconsistent. In this meta-analysis, we seek to investigate the relationship between GSTM1 and GSTT1 polymorphisms and the risk of EC. We searched Medline, PubMed, Web of Science, Embase, Chinese National Knowledge Infrastructure database, and Chinese Biomedical Literature database to identify eligible studies. The pooled odds ratios (ORs) with 95% confidence intervals (CIs) for the association were determined using a fixed- or random-effect model. Tests for heterogeneity of the results and sensitivity analyses were performed. A total of six case-control studies were included in the final meta-analysis of GSTM1 (1293 cases and 2211 controls) and GSTT1 (1286 cases and 2200 controls) genotypes. Overall, GSTM1 null genotype was not significantly associated with an increased risk of EC (OR = 1.00, 95% CI = 0.76-1.30, = 0.982). Similarly, for GSTT1 deletion genotype, we observed no association under the investigated model in the overall analysis (OR = 0.91, 95% CI = 0.64-1.30, = 0.619). Subgroup analysis also showed no significant association between the GSTM1 null genotype and EC risk in hospital-based design (OR = 1.26, 95% CI = 0.93-1.71, = 0.131) and no relationship between GSTT1 null genotype with EC risk in population-based design (OR = 1.18, 95% CI = 0.79-1.76, = 0.407). However, GSTM1 null genotype contributed to an increased EC risk in population-based design (OR = 0.76, 95% CI = 0.60-0.97, = 0.027), while null GSTT1 in hospital-based studies (OR = 0.70, 95% CI = 0.52-0.93, = 0.015). The present meta-analysis suggested that GSTs genetic polymorphisms may not be involved in the etiology of EC. Large epidemiological studies with the combination of GSTM1 null, GSTT1 null, and design-specific with the development of EC are needed to prove our findings.
谷胱甘肽S-转移酶M1（GSTM1）和T1（GSTT1）基因的遗传多态性与子宫内膜癌（EC）风险之间关联的流行病学证据并不一致。在这项荟萃分析中，我们旨在研究GSTM1和GSTT1基因多态性与EC风险之间的关系。我们检索了Medline、PubMed、科学网、Embase、中国知网数据库和中国生物医学文献数据库，以确定符合条件的研究。使用固定效应或随机效应模型确定关联的合并比值比（OR）及其95%置信区间（CI）。对结果进行异质性检验和敏感性分析。共有六项病例对照研究纳入了GSTM1（1293例病例和2211例对照）和GSTT1（1286例病例和2200例对照）基因型的最终荟萃分析。总体而言，GSTM1缺失基因型与EC风险增加无显著关联（OR = 1.00，95%CI = 0.76 - 1.30，P = 0.982）。同样，对于GSTT1缺失基因型，在总体分析的研究模型下我们未观察到关联（OR = 0.91，95%CI = 0.64 - 1.30，P = 0.619）。亚组分析还显示，在基于医院的设计中，GSTM1缺失基因型与EC风险之间无显著关联（OR = 1.26，95%CI = 0.93 - 1.71，P = 0.131），在基于人群的设计中，GSTT1缺失基因型与EC风险之间无关联（OR = 1.18，95%CI = 0.79 - 1.76，P = 0.407）。然而，在基于人群的设计中，GSTM1缺失基因型会增加EC风险（OR = 0.76，95%CI = 0.60 - 0.97，P = 0.027），而在基于医院的研究中，GSTT1缺失基因型会增加EC风险（OR = 0.70，95%CI = 0.52 - 0.93，P = 0.015）。目前的荟萃分析表明，谷胱甘肽S-转移酶基因多态性可能不参与EC的病因学。需要结合GSTM1缺失、GSTT1缺失以及特定设计与EC发生情况的大型流行病学研究来证实我们的发现。
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