Journal
ENDOCRINOLOGY AND METABOLISM CLINICS OF NORTH AMERICA
Volume 40, Issue 3, Pages 625-+Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.ecl.2011.05.013
Keywords
Prostate cancer; Hormone refractory; Castration resistant; Androgen ablation; Steroidogenesis; Intracrine; Abiraterone
Categories
Funding
- Prostate Cancer Foundation
- National Institutes of Health [K23 CA122820]
- Damon Runyon Cancer Research Foundation [CI-40-08]
- Pacific Northwest Prostate Cancer SPORE [P50 CA097186]
- Veterans Affairs Research Service
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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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