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Clin Cancer Res 51-6362 Hearn, Jason W D; Abu Ali, Ghada; Reichard, Chad A et al.(2016) HSD3B1 and resistance to androgen-deprivation therapy in prostate cancer: a retrospective, multicohort study.
Androgen deprivation therapy by depletion of gonadal testosterone is the upfront standard therapy for advanced disease.
Metastatic disease almost invariably recurs as castration-resistant prostate cancer (CRPC), which is the lethal form of this disease.
Although the majority of patients with CRPC respond to abiraterone acetate, a subset do not have any initial response and nearly all responding tumors will eventually acquire resistance.
A recent discovery that has been clinically validated has demonstrated that conversion from adrenal precursor steroids to dihydrotestosterone (DHT), the most potent androgen that drives CRPC progression, unexpectedly bypasses testosterone.
In Aim 3, the consequences of wild-type and mutant 3HSD1 interaction will be assessed.
The ultimate anticipated benefit of this proposal is the identification of a first-in-clas gain-of-function mutation in a steroidogenic enzyme in CRPC that may serve as a biomarker of response or resistance to hormonal therapies, including abiraterone acetate.
Although originally developed for elucidating the relationship between religiousness and health outcomes in children and youths, most of the theoretical contents could be adopted as a paradigm to delineate the relationship between religiousness and mental health in various populations.
From such undeniable testimony did the practised woodsman arrive at the truth, with nearly as much certainty and precision as if he had been a witness of all those events which his ingenuity so easily elucidated.
Prostate cancer is the most common cause of cancer and second leading cause of cancer death for men in the United States.
Localized disease is potentially curable with radiation or surgery; however, advanced disease remains incurable.
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