Xinyang Liu1, Xiaowei Zhang1, Zhichao Wang2, Jinjia Chang1, Zheng Wu1, Zhe Zhang1, Shanshan Wang1, Jin Li3. 1. Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai 200032, China. 2. Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai 200032, China. 3. Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai 200032, China; Department of Oncology, Shanghai Medical College, Shanghai 200032, China. Email: fudanlijin@163.com.
Abstract
BACKGROUND: The pathogenesis of gastric cancer (GC) involves environmental and genetic factors. Recently, two genome-wide association studies found that phospholipase C epsilon 1 (PLCE1) polymorphisms might be related to GC risk, and several studies further validated this finding. However, these studies yielded inconsistent results. METHODS: A comprehensive database search was performed to identify eligible studies. Odds ratios with 95% confidence intervals were calculated to assess the strength of the association between PLCE1 rs2274223, rs753724, and rs11187842 and risk of GC. Subgroup analyses, publication bias, and sensitivity analyses were also conducted. RESULTS: Eleven studies (12 cohorts) were included in the meta-analysis. Based on 13 676 cases and 23 569 controls, a significant association between PLCE1 rs2274223 and GC risk was detected under various genotypic models. In the subgroup analyses, the association was significant for cardia GC, but weak for non-cardia GC. The association under the heterozygote model was detected for PLCE1 rs753724 and rs11187842 based on three studies involving 2768 cases and 3890 controls. CONCLUSIONS: Our findings demonstrate that the presence of the G allele at rs2274223 of the PLCE1 gene may contribute to susceptibility to GC, especially cardia GC. PLCE1 rs753724 and rs11187842 are associated with GC risk under the heterozygote model. Further well-designed large studies are warranted to validate these findings.
BACKGROUND: The pathogenesis of gastric cancer (GC) involves environmental and genetic factors. Recently, two genome-wide association studies found that phospholipase C epsilon 1 (PLCE1) polymorphisms might be related to GC risk, and several studies further validated this finding. However, these studies yielded inconsistent results. METHODS: A comprehensive database search was performed to identify eligible studies. Odds ratios with 95% confidence intervals were calculated to assess the strength of the association between PLCE1rs2274223, rs753724, and rs11187842 and risk of GC. Subgroup analyses, publication bias, and sensitivity analyses were also conducted. RESULTS: Eleven studies (12 cohorts) were included in the meta-analysis. Based on 13 676 cases and 23 569 controls, a significant association between PLCE1rs2274223 and GC risk was detected under various genotypic models. In the subgroup analyses, the association was significant for cardia GC, but weak for non-cardia GC. The association under the heterozygote model was detected for PLCE1rs753724 and rs11187842 based on three studies involving 2768 cases and 3890 controls. CONCLUSIONS: Our findings demonstrate that the presence of the G allele at rs2274223 of the PLCE1 gene may contribute to susceptibility to GC, especially cardia GC. PLCE1rs753724 and rs11187842 are associated with GC risk under the heterozygote model. Further well-designed large studies are warranted to validate these findings.