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Polymorphism in the Androgen Biosynthesis Gene (CYP17), a Risk for Prostate Cancer

A Meta-Analysis

Bibliographic Data

ID21748540
AuthorsClement Yaw Effah (0000-0002-9095-4558, Zhengzhou University), Ling Wang (0000-0002-5015-7706, Zhengzhou University), Clement Agboyibor (0000-0002-2519-9146, Zhengzhou University), Emmanuel Kwateng Drokow (0000-0002-7363-9281, Department of Radiation Oncology, Zhengzhou University People’s Hospital & Henan Provincial People’s Hospital Henan, China), Songcheng Yu (0000-0002-4486-3962, Zhengzhou University), Wei Wang (0000-0001-5806-2368, Zhengzhou University), Yongjun Wu (0000-0002-1212-6511, Zhengzhou University)
Year2020
Volume14
Issue5
Publication date2020-09-01
Peer ReviewedYes
Open AccessYes
TypeARTICLE
VenueAmerican Journal of Men s Health (JOURNAL)
Journal identifiersISSN: 1557-9883 • E-ISSN: 1557-9891
PublisherSAGE Publications (PUBLISHER • US)
DOI10.1177/1557988320959984
LanguageEN
References cited24

Gene polymorphism is one of the few factors that increases the risk of prostate cancer. T to C substitution in the 5’ promoter region of the CYP17 gene is hypothesized to increase the rate of gene transcription, increase androgen production, and thereby increase the risk of prostate cancer. Nevertheless, the inconsistencies originating from studies on CYP17 polymorphism and prostate cancer prompted this meta-analysis, to decipher the association between CYP17 polymorphism and prostate cancer. Most case-control studies addressing CYP17 polymorphism and prostate cancer were exhaustively searched from Web of Science, Google Scholar, and PubMed. The various genotype distributions as well as the minor allele distributions were retrieved. Pooled odds ratios ( ORs) with their 95% CI and estimates of the Hardy–Weinberg Equilibrium were calculated. Analyses were performed using the RevMan v.5.3 software and SPSS v.21. There was high-pooled heterogeneity ( I 2 = 87.0%, OR = .42, CI [.39, .45], and p

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