Role of CD152 genetic polymorphisms in the susceptibility to breast cancer

被引:5
作者
Chen, Hai [1 ]
Qi, Xiaodong [1 ]
Bai, Xue [1 ]
Qiu, Ping [1 ]
Chen, Bin [1 ]
机构
[1] Gen Hosp Beijing Mil Command, Dept Galactophore, Beijing 100000, Peoples R China
关键词
CD152; CTLA-4; polymorphisms; breast cancer; immune response; CTLA-4; POLYMORPHISMS; AUTOIMMUNITY; ASSOCIATION; PROGRESSION; STATISTICS; BLOCKADE; WOMEN; RISK;
D O I
10.18632/oncotarget.15794
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background: The polymorphisms in cluster of differentiation 152 (CD152) gene have been reported to be associated with breast cancer (BC), but relevant findings were far from conclusive. Therefore, we carried out this meta-analysis to combine those results for a clearer perspective on this issue. Results: In our meta-analysis, a total of 8 eligible publications of 19 case-control studies were selected, which totally contained 7,442 BC cases and 7,376 normal controls. Among the five polymorphisms of CD152 gene, + 49 G/A,-1661 A/G and -318 C/T significantly increased the risk of BC under corresponding genetic comparisons; while CT60 G/A polymorphism was negatively related to the cancer susceptibility. In addition,-1772 T/C polymorphism of CD152 gene was not associated with the development of BC. Materials and methods: Online databases and other sources were searched for published studies on the relationship between BC susceptibility and CD152 polymorphisms (+ 49 G/A,-1661 A/G,-1722 T/C,-318 C/T and CT60 G/A). The strength of association was evaluated with pooled odds ratios (ORs) and their corresponding 95% confidence intervals (95% CIs). Heterogeneity evaluation was conducted via Q test. Sensitivity analysis was used to detect the stability of our results. Begg's funnel plot and Egger's test were applied to investigate publication bias among selected studies. Conclusions: The polymorphisms + 49 G/A,-1661 A/G and -318 C/T may elevate the susceptibility to BC, but the polymorphism CT60 G/A may offer protection against the cancer.
引用
收藏
页码:26679 / 26686
页数:8
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