Resistance is also mediated by non-canonical pathways, such as ROR-γ (retinoic acid receptor-related orphan receptor γ), which acts as a driver of AR expression in CRPC.
Antiandrogen treatment can cause stromal cell reprogramming, leading to SPP1+ myCAFs (myofibroblastic cancer-associated fibroblasts) that create a microenvironment resistant to androgen deprivation therapy.
Key findings regarding androgen-targeted therapy resistance:
Based on recent research into prostate cancer treatment, remains a key target, but therapy resistance (specifically, castration-resistant prostate cancer, or CRPC) is a major challenge. Research highlights that, while standard treatments like enzalutamide or abiraterone are used, tumor resistance often emerges through the adaptation of AR variants (e.g., AR-V7 , ARv567es ).
While potent AR inhibitors are used, they can force tumors to de-differentiate into AR-negative disease. For more specific information, pleaseg., ARv567es or AR-V7) The effect of specific drugs (e.g., enzalutamide) The role of ROR-γ in treatment resistance To narrow this down, Clinical trial outcomes for resistance? A summary of new therapeutic targets being researched?