Despite castrate levels of androgens, the androgen receptor (AR) remains active and continues to drive prostate cancer progression. Since the approval of docetaxel, four additional agents that show a survival benefit have been registered on the basis of randomized phase 3 trials. These have included enzalutamide and abiraterone, two agents designed specifically to affect the androgen axis, sipuleucel-T, which stimulates the immune system and cabazitaxel, a chemotherapeutic agent. Denosumab was shown to significantly delay skeletal-related events. Clinicians are challenged with a multitude of treatment options and potential sequencing of these agents that, consequently, make clinical decision making more complex. The induction of constitutively-active AR splice variants (AR-Vs) driving clonal proliferation of AR-negative and AR-independent metastases may be one major potential mechanism of resistance to new hormone therapies.
Keywords: AR-V7; Abiraterone acetate; Acétate d’abiratérone; Alpharadin; Cabazitaxel; Cancer de prostate résistant à la castration; Denosumab; Docetaxel; Docétaxel; Dénosumab; Enzalutamide; Metastatic castration-resistant prostate cancer; Sipuleucel-T; Splicing variants; Variants épissage.
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