Research Papers:

Systematic meta-analyses of gene-specific genetic association studies in prostate cancer

Qiang Hao, Dong Wei, Yaoguang Zhang, Xin Chen, Fan Yang, Ze Yang, Xiaoquan Zhu and Jianye Wang _

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Oncotarget. 2016; 7:22271-22284. https://doi.org/10.18632/oncotarget.7926

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Qiang Hao1,2,3, Dong Wei2, Yaoguang Zhang2, Xin Chen2, Fan Yang3, Ze Yang3, Xiaoquan Zhu3, Jianye Wang1,2,3

1Graduate School of Peking Union Medical College, Beijing, 100730, China

2Department of Urology, Beijing Hospital, Beijing, 100730, China

3Key Laboratory of Geriatrics, Beijing Hospital and Beijing Institute of Geriatrics, Ministry of Health, Beijing, 100730, China

Correspondence to:

Jianye Wang, e-mail: [email protected]

Xiaoquan Zhu, e-mail: [email protected]

Keywords: prostate cancer, susceptibility, single nucleotide variant, meta-analyses

Received: December 22, 2015    Accepted: February 23, 2016    Published: March 05, 2016


In the past twenty-five years, over 700 case-control association studies on the risk of prostate cancer have been published worldwide, but their results were largely inconsistent. To facilitate following and explaining these findings, we performed a systematic meta-analysis using allelic contrasts for gene-specific SNVs from at least three independent population-based case-control studies, which were published in the field of prostate cancer between August 1, 1990 and August 1, 2015. Across 66 meta-analyses, a total of 20 genetic variants involving 584,100 subjects in 19 different genes (KLK3, IGFBP3, ESR1, SOD2, CAT, CYP1B1, VDR, RFX6, HNF1B, SRD5A2, FGFR4, LEP, HOXB13, FAS, FOXP4, SLC22A3, LMTK2, EHBP1 and MSMB) exhibited significant association with prostate cancer. The average summary OR was 1.33 (ranging from: 1.016–3.788) for risk alleles and 0.838 (ranging from: 0.757–0.896) for protective alleles. Of these positive variants, FOXP4 rs1983891, LMTK2 rs6465657 and RFX6 rs339331 had not been previously meta-analyzed. Further analyses with sufficient power design and investigations of the potential biological roles of these genetic variants in prostate cancer should be conducted.

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