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More evidence intratumoral DHT synthesis drives castration-resistant prostate cancer
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More evidence intratumoral DHT synthesis drives castration-resistant prostate cancer
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More evidence intratumoral DHT synthesis drives castration-resistant prostate cancer
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Journal Article
More evidence intratumoral DHT synthesis drives castration-resistant prostate cancer
2014
Overview
Again-of-function stabilizing somatic mutation in 3β-hydroxysteroiddehydrogenase type 1 （3βHSDI, HSD3B1） was reported in castration-resistant prostate cancer. The A-C nucleotide polymorphism replaced asparagine-367 with threonine （3βHSD1-N367T） as a homozygous somatic mutation in a subset of castration-resistant prostate cancers by loss of heterozygosity of the wild-type allele. Increased stability of 3[HSD I-N367T was associated with decreased ubiquitin-mediated degradation and higher levels of dihydrotestosterone （DHT）. The studies suggest that genetic instability in castration-resistant prostate cancer favors the more stable 313HSD I-N367T mutant that contributes to drug resistance. A somatic mutation in a steroid metabolic enzyme required for DHT synthesis provides further support for intratumoral androgen synthesis contributing to prostate cancer progression.
Publisher
Medknow Publications & Media Pvt. Ltd,Medknow Publications & Media Pvt Ltd,Wolters Kluwer Medknow Publications
Subject
