Abstract Prostate cancer development and treatment has been associated with steroid hormones and/or steroid metabolites. While consensus seems to be building that serum testosterone levels are not related to disease risk, the role of genes involved in steroid metabolism have not been extensively studied. The UDP-glucuronosyltransferase (UGT) enzymes are part of a superfamily of genes involved in phase II detoxification of a wide variety of endogeneous and exogenous substances including bile, odorants, steroids, and drugs. The UGT2B17 gene is expressed in the prostate where it catalyzes the conjugation of a glucuronic acid moiety to steroids such as androstane-3α, 17βdiol. Several studies have examined whether a copy number variant (CNV) of UGT2B17 is associated with prostate cancer risk in case control studies, however, results have been inconclusive, and only one of the studies included African Americans. We examined the relationship of UGT2B17 CNV with prostate cancer risk aggressiveness in a hospital-based, case-control study conducted at the Durham Veterans Administration Hospital, and the relationship between serum levels of the glucuronide of androstane-3α, 17βdiol, AAG, in healthy Caucasians and African Americans. Levels of AAG were measured using ELISA. UGT2B17 genotype was determined by gene-specific copy number assays using Taqman Realtime PCR which showed 0, 1, or 2 alleles of the gene. Whereas CNV was not related to race (p=0.85), a higher CNV was significantly associated with higher androstane-3α, 17βdiol levels in healthy white men (p=0.018) but not non-white men (p=0.94). We found no association between CNV and cancer risk among all men (p=0.59) nor when stratified by white (p=0.70) vs. non-white (p=0.72). Among men with cancer, CNV was not related to Gleason score (p=0.32). These findings suggest that CNV may be associated with serum hormones levels, and these associations may differ between white and non-white men. Serum levels may be altered by other genetic or epigenetic factors in non-white populations. The role of CNV as a risk factor for prostate cancer requires further study in larger samples and with genetic and epigenetic variants. Funded by Department of Defense, NIH NCMHD P20 MD000175, S06-GM008049-33 Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2770. doi:10.1158/1538-7445.AM2011-2770