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Commonly used therapies for prostate cancer (PC) that block androgen receptor (AR) signaling inhibit regrowth, but aggressive castrate-resistant (CR)PC abrogates anti-androgen therapy. Recently published data shows that glucocorticoid receptor (GR) can drive the growth of CRPC when AR is blocked, by mimicking AR activity. Due to the evolution of CRPC into a more invasive disease, we hypothesized that GR-driven CRPC has different activities than AR that promote progression to metastatic disease.doi:10.14293/s2199-1006.1.sor-.ppk9xz7.v1 fatcat:og44ovvj3ve53g7w3vsb4bkryy