Association between the RAD51 135 G>C polymorphism and risk of cancer: a meta-analysis of 19,068 cases and 22,630 controls

RAD51 135G>C can modify promoter activity and the penetrance of BRCA1/2 mutations, which plays vital roles in the etiology of various cancer. To date, previous published data on the association between RAD51 135G>C polymorphism and cancer risk remained controversial. Recent meta-analysis only...

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Published inPloS one Vol. 8; no. 9; p. e75153
Main Authors Wang, Wei, Li, Jia-Lin, He, Xiao-Feng, Li, An-Ping, Cai, Yong-Lin, Xu, Na, Sun, Shu-Mei, Wu, Bing-Yi
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 09.09.2013
Public Library of Science (PLoS)
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Summary:RAD51 135G>C can modify promoter activity and the penetrance of BRCA1/2 mutations, which plays vital roles in the etiology of various cancer. To date, previous published data on the association between RAD51 135G>C polymorphism and cancer risk remained controversial. Recent meta-analysis only analyzed RAD51 135G>C polymorphism with breast cancer risk, but the results were also inconsistent. A meta-analysis based on 39 case-control studies was performed to investigate the association between cancer susceptibility and RAD51 135G>C. Odds ratios (OR) with 95% confidence intervals (CIs) were used to assess the association in different inheritance models. Heterogeneity among studies was tested and sensitivity analysis was applied. Overall, no significant association was found between RAD51 135G>C polymorphism and cancer susceptibility in any genetic model. In further stratified analysis, significantly elevated breast cancer risk was observed in BRCA2 mutation carriers (recessive model: OR = 4.88, 95% CI = 1.10-21.67; additive model: OR = 4.92, 95% CI = 1.11-21.83). This meta-analysis suggests that RAD51 variant 135C homozygote is associated with elevated breast cancer risk among BRCA2 mutation carriers. Moreover, our work also points out the importance of new studies for RAD51 135G>C association in acute myeloid leukemia, especially in Caucasians, where at least some of the covariates responsible for heterogeneity could be controlled, to obtain a more conclusive understanding about the function of the RAD51 135G>C polymorphism in cancer development.
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Conceived and designed the experiments: BYW. Performed the experiments: WW JLL. Analyzed the data: XFH APL. Contributed reagents/materials/analysis tools: YLC NX SMS. Wrote the paper: WW JLL. Data acquisition: XFH APL YLC NX SMS. Manuscript editing and final version approval: BYW.
Competing Interests: The authors declare some authors worked in Shanxi Zhendong Pharmaceutical Co. Ltd. after their graduation. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0075153