Article Abstract

Does increased expression of glucocorticoid receptor support application of antagonists to this receptor for the treatment of castration resistant prostate cancer?

Authors: Yukiyoshi Hirayama, Marianne D. Sadar

Abstract

Despite the development of potent second generation therapeutic agents targeting the androgen receptor (AR) pathway for castration resistant prostate cancer (CRPC), the disease eventually acquires resistance to these therapies after an initial response. Multiple mechanisms of resistance have been proposed including gain-of-function mutations in AR ligand-binding domain (LBD), expression of constitutively active AR splice variants, and more recently increased expression of glucocorticoid receptor (GR) and progesterone receptor (PR) (1).