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Design and end points of clinical trials for patients with progressive prostate cancer and castrate levels of testosterone: recommendations of the Prostate Cancer Clinical Trials Working Group.
TLDR
New consensus criteria for eligibility and outcome measures in trials that evaluate systemic treatment for patients with progressive prostate cancer and castrate levels of testosterone are defined, with increasing emphasis on time-to-event end points as decision aids in proceeding from phase II to phase III trials.
Increased expression of genes converting adrenal androgens to testosterone in androgen-independent prostate cancer.
TLDR
Enhanced intracellular conversion of adrenal androgens to testosterone and dihydrotestosterone is a mechanism by which prostate cancer cells adapt to androgen deprivation and suggest new therapeutic targets.
Mutation of the androgen-receptor gene in metastatic androgen-independent prostate cancer.
TLDR
Functional studies of two of the mutant androgen receptors demonstrated that they could be activated by progesterone and estrogen, and may provide a selective growth advantage after androgen ablation.
Eligibility and response guidelines for phase II clinical trials in androgen-independent prostate cancer: recommendations from the Prostate-Specific Antigen Working Group.
TLDR
The purpose of determining the number of patients whose PSA level drops in a phase II trial of AIPC is to guide the selection of agents for further testing and phase III trials and developed practical guidelines for using PSA as a measurement of outcome.
Biology of prostate-specific antigen.
TLDR
Serum total PSA levels are increased in PCa, and PSA screening has dramatically altered PCa presentation and management, and recent data indicate that there may be additional roles for PSA in the pathogenesis of PCa.
Selection for androgen receptor mutations in prostate cancers treated with androgen antagonist.
TLDR
Findings demonstrate that AR mutations occur in response to strong selective pressure from flutamide treatment, and these mutations responded to subsequent treatment with bicalutamide, an AR antagonist that blocks the mutant ARs.
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