Background: Patients with PC have limited treatment options after failure of hormonal and taxane therapy. Androgen receptor (AR) signaling may exert therapeutic effects on the DNA repair pathway in PC. We have assessed the proteomic/genomic DNA repair aberrations in primary (P) and metastatic (M) PC and explored the therapeutic
implications of these mutations using panomic next generation sequencing (NGS). We hypothesized that there is a differential in gene expression and mutation between P and M tumors.