Philip A. Watson

TL;DR: The diarylthiohydantoins RD162 and MDV3100 are characterized, two compounds optimized from a screen for nonsteroidal antiandrogens that retain activity in the setting of increased androgen receptor expression that appear to be promising candidates for treatment of advanced prostate cancer.

TL;DR: This Review highlights emerging mechanisms of acquired resistance to contemporary therapies targeting the AR pathway, which fall into the three broad categories of restored AR signalling, AR bypass signalling and complete AR independence.

TL;DR: In vitro and in vivo human prostate cancer models are used to show that these tumors can develop resistance to the antiandrogen drug enzalutamide by a phenotypic shift from androgen receptor–dependent luminal epithelial cells to AR-independent basal-like cells.

TL;DR: In this article, ligand-independent androgen receptor splice variants lacking the ligand binding domain (ARVs), originally isolated from prostate cancer cell lines derived from a single patient, are detected in normal and malignant human prostate tissue, with the highest levels observed in late stage, castration resistant prostate cancer.

TL;DR: It is demonstrated that the androgen receptor (AR) regulates a transcriptional program of DNA repair genes that promotes prostate cancer radioresistance, providing a potential mechanism by which androgen deprivation therapy synergizes with ionizing radiation.