Clinical Research Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N, D4-100, Seattle, WA, USA.
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.
Mostaghel EA, Plymate S. Are you the author?
Reference: Endocrinol Metab Clin North Am. 2011 Sep;40(3):625-42.