contribution of the -160ca polymorphism in the e-cadherin promoter to cancer risk a meta-analysis of 47 case-control studies贡献的-160 ca的钙粘蛋白启动子多态性癌症风险47个病例对照研究的荟萃分析.pdfVIP

contribution of the -160ca polymorphism in the e-cadherin promoter to cancer risk a meta-analysis of 47 case-control studies贡献的-160 ca的钙粘蛋白启动子多态性癌症风险47个病例对照研究的荟萃分析.pdf

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contribution of the -160ca polymorphism in the e-cadherin promoter to cancer risk a meta-analysis of 47 case-control studies贡献的-160 ca的钙粘蛋白启动子多态性癌症风险47个病例对照研究的荟萃分析

Contribution of the -160C/A Polymorphism in the E- cadherin Promoter to Cancer Risk: A Meta-Analysis of 47 Case-Control Studies 1. 1. 2 1 1 Lin Wang , Guiying Wang , Chenqi Lu , Bo Feng *, Jiuhong Kang * 1 Endocrinology Department, Shanghai East Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, Shanghai, People’s Republic of China, 2 Laboratory of Population and Quantitative Genetics, Institute of Biostatistics, SKLGE, School of Life Sciences, Fudan University, Shanghai, People’s Republic of China Abstract Background: The -160C/A polymorphism (rs16260) of E-cadherin, a tumor repressor gene, has been shown to be a tumor susceptibility allele for various types of cancers. Because the significance of this polymorphism to cancer risk has been recognized, there are increasing studies investigating -160C/A in different types of cancers and ethnic populations. However, there is still uncertainty about the level of risk for a variety of cancers. Methods: To resolve the controversial question raised by these studies as of March 2012 and provide more statistical power for detecting the significance of -160C/A, we performed a meta-analysis of 47 case-control studies in 16 types of cancers (18,194 cases and 20,207 controls). A meta-regression model and subgroup analysis were employed to identify the source of heterogeneity. Publication bias was evaluated, and sensitivity analysis and cumulative evidence assessment were also performed. Results: Using fixed- and random-effects models, the -160AA homozygote was more susceptible to urothelial cancer compared with the -160CA heterozygote. Additionally, the -160A allele is an ethnic

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