UGT2B28 – Prostate Cancer

The evidence evaluating the association between UGT2B28 and prostate cancer is currently disputed. Two independent case‑control studies, involving a combined total of 426 subjects (PMID:20056642, PMID:28882566), analyzed copy number variations (CNVs) and single‑nucleotide polymorphisms (SNPs) within several genes related to dihydrotestosterone metabolism. In both investigations, UGT2B28 variants did not show a statistically significant association with prostate cancer risk, even though other genes in the pathway revealed some variation in risk estimates. Furthermore, no familial segregation or recurrent pathogenic variants were identified for UGT2B28. The absence of corroborative genetic evidence is compounded by functional studies, which, while supportive of a role for other UGT isoforms in metabolism, did not provide experimental support for the involvement of UGT2B28 in prostate cancer pathogenesis. Overall, the current data do not validate a clinically actionable association for UGT2B28 with prostate cancer risk.

Key take‑home sentence: Despite a plausible biological role in steroid metabolism, existing genetic and functional evidence disputes a meaningful contribution of UGT2B28 to prostate cancer, limiting its current utility in diagnostics and commercial testing.

References

• Cancer epidemiology, biomarkers & prevention • 2010 • Genetic variation of genes involved in dihydrotestosterone metabolism and the risk of prostate cancer PMID:20056642
• Gene • 2017 • Genetic variations in UGT2B28, UGT2B17, UGT2B15 genes and the risk of prostate cancer: A case‑control study PMID:28882566

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