Continued activation of the androgen receptor (AR) axis despite castration remains a critical force in the development of castration-resistant prostate cancer (CRPC). Therapeutic strategies designed to more effectively ablate tumoral androgen activity are required to improve clinical efficacy and prevent disease progression. Tumor-based alterations in expression and activity of the AR and in steroidogenic pathways mediating ligand generation facilitate the development of CRPC. This article reviews AR and ligand-dependent mechanisms underlying CRPC progression and the status of novel hormonal therapies targeting the AR axis that are currently in clinical and preclinical development.
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