Abstract Longitudinal plasma cfDNA profiling from the phase 3 Alliance A031201 trial revealed divergent resistance trajectories in mCRPC. Rapid progressors harbored non-AR alterations suggesting intrinsic resistance, whereas delayed progressors showed progressive AR amplifications, structural rearrangements and extrachromosomal DNA–associated evolution. These findings support biomarker-guided strategies targeting AR-dependent and AR-independent disease states.
Chauhan et al. (Fri,) studied this question.