Objective. Recent studies on the association between uridine diphosphosglucuronosyltransferases (UGTs) 2B17 polymorphism and risk of prostate cancer (PCa) showed inconclusive results. To clarify this possible association, we conducted a meta-analysis of published studies. Methods. We searched the published literature from PubMed, Embase, Google Scholar, and China National Knowledge Infrastructure (CNKI). According to our inclusion criteria, studies that observed the association between UGT2B17 polymorphism and PCa risk were included. The principal outcome measure was the adjusted odds ratio (OR) with 95% confidence interval (CI) for the risk of PCa associated with UGT2B17 polymorphism. Results. A total of 6 studies with 7,029 subjects (3,839 cases and 3,190 controls) were eligible for inclusion in the meta-analysis. Overall, there was a significant association between UGT2B17 polymorphism and increased risk of prostate cancer ( , 95% CI 1.14–2.64, ). Similar results were found in the subgroup analyses by ethnicity and types of controls. Conclusion. This meta-analysis demonstrates that UGT2B17 polymorphism is associated with prostate cancer susceptibility, and it contributes to the increased risk of prostate cancer. 1. Introduction Prostate cancer is the fourth most common cancer in men, comprising approximately one-eighth of all male-specific cancers in the world [1]. Identifying risk factors for prostate cancer is critically important to develop potential interventions and to expand our understanding of the biology of this disease [2, 3]. The etiology of prostate cancer remains unknown, but race, age, family history of prostate cancer, and steroid hormone levels have been suggested as contributing factors [4]. The literature has revealed that eunuchs (men lacking testosterone) do not develop prostate cancer [5], generating the theory that testosterone plays a vital role in the development and progression of the disease. As a corollary, testis ablation is a well-established and effective way to stop progression of the disease [6]. Androgens, responsible for the healthy growth and maintenance of the prostate, are steroid hormones expressed in the prostate [7]. The two main types of androgens found in males, testosterone and dihydrotestosterone (DHT), have been postulated to modify the risk of prostate cancer [8, 9]. Most epidemiologic studies of prostate cancer have focused on the genes involved in the steroidogenic pathway, such as P450 cytochrome 3A4 (CYP3A4), CYP17, and SRD5A2. Although differences in androgen levels may also reflect variations in
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