Genomic Alterations in Cell-Free DNA and Enzalutamide Resistance in Castration-Resistant Prostate Cancer

Abstract

Prostate cancer cells are initially reliant on circulating androgens binding and activating the endogenous androgen receptor (AR). Although androgen deprivation therapy elicits a response in most patients, progression to castration-resistant prostate cancer (CRPC), driven frequently by AR reactivation, is inevitable.¹ However, in recent years, continued targeting of the AR signaling axis with abiraterone acetate and enzalutamide has changed clinical practice and improved the overall survival of patients with CRPC.^2-5 Multiple other AR axis inhibitors are in clinical trials, promising to expand the arsenal available to patients.⁶