Oncotarget

Reviews:

Association between BRCA1 P871L polymorphism and cancer risk: evidence from a meta-analysis

Limin Miao, Yang Yu, Yefeng Ji, Bo Zhang, Zhiyao Yuan, Yifei Du, Longbiao Zhu, Ruixia Wang, Ning Chen and Hua Yuan _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2017; 8:30587-30594. https://doi.org/10.18632/oncotarget.15739

Metrics: PDF 1806 views  |   HTML 1937 views  |   ?  


Abstract

Limin Miao1,*, Yang Yu1,*, Yefeng Ji1, Bo Zhang1, Zhiyao Yuan1, Yifei Du1, Longbiao Zhu1, Ruixia Wang1, Ning Chen1,2 and Hua Yuan1,2

1 Jiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, China

2 Department of Oral and Maxillofacial Surgery, Affiliated Hospital of Stomatology, Nanjing Medical University, Nanjing, China

* These authors have contributed equally to this work

Correspondence to:

Hua Yuan, email:

Keywords: BRCA1, polymorphism, cancer risk, meta-analysis

Received: November 09, 2016 Accepted: February 13, 2017 Published: February 25, 2017

Abstract

Breast cancer 1 (BRCA1) gene makes great contributions to the repair of DNA. The association between BRCA1 P871L polymorphism and cancer risk has been investigated in a growing number of studies, but the conclusions are not conclusive. To obtain a comprehensive conclusion, we performed a meta-analysis of 24 studies with 13762 cases and 22388 controls. The pooled results indicated that BRCA1 gene P871L variant decreased risk of overall cancer (homozygous model: odds ratio (OR) = 0.89, 95%confidence interval (CI) = 0.79-1.00; recessive model: OR = 0.89, 95% CI = 0.80-0.99). The stratified analysis observed decreased risk associated with BRCA1 P871L in subgroups among Asians and high score studies, but not Caucasians or low score studies. In conclusion, despite several limitations, this meta-analysis suggested that BRCA1 P871L genetic variation may be associated with decreased susceptibility to cancer.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 15739