Deletion polymorphism of the UGT2B17 gene is associated with increased risk for prostate cancer and correlated to gene expression in the prostate
A-H Karypidis, M Olsson, S-O Andersson, Anders Rane, Lena Ekstrom
The Pharmacogenomics Journal2008 (online Mar 2007)
Summary (paraphrased)
UGT2B17 is a highly prostate-abundant UDP- glucuronosyltransferase with strong activity against androgens, and its deletion had previously been linked to low or undetectable urinary testosterone. The authors quantified UGT2B17 mRNA in normal prostate tissue by genotype and tested the deletion in a Swedish population-based case-control study (176 prostate cancer cases, 161 controls). Insertion-allele homozygotes expressed roughly 30 times more UGT2B17 mRNA in prostate tissue than heterozygotes, and deletion carriers had significantly increased prostate cancer risk (OR 2.07, 95% CI 1.32-3.25). The authors conclude the deletion polymorphism shapes androgen glucuronidation capacity in target tissue and associates with prostate cancer risk.
Why it’s in the systems review
UGT2B17 is the single gene Powers names most prominently — his theorized "base, core defect," later reframed as a risk modifier — and this is human association data showing that its deletion changes androgen handling inside a steroid target tissue and tracks with an androgen-driven disease outcome. It is the natural companion to the corpus's Yang 2008 (UGT2B17 copy number and circulating testosterone/estradiol) and belongs in any causal-pathway diagram of how impaired steroid clearance could leave a vulnerable endocrine milieu after 5-ARI exposure.
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