Androgen receptor genomic alterations and treatment resistance in metastatic prostate cancer

Genomic alterations to the androgen receptor (AR) are common in metastatic castration‐resistant prostate cancer (mCRPC). AR copy number amplifications, ligand‐binding domain missense mutations, and intronic structural rearrangements can all drive resistance to approved AR pathway inhibitors and their detection via tissue or liquid biopsy is linked to clinical outcomes. With an increasingly crowded treatment landscape, there is hope that AR genomic alterations can act as prognostic and/or predictive biomarkers to guide patient management.