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Testosterone boosts for treatment of castration resistant prostate cancer: An experimental implementation of intermittent androgen deprivation

The primary therapeutic target for non‐organ‐confined prostate cancer is the androgen receptor (AR). Main strategies to ablate AR function are androgen depletion and direct receptor blockade by AR antagonists. However, incurable castration resistant prostate cancer (CRPC) develops resistance mechanisms to cope with trace amounts of androgen including AR overexpression and mutation in the AR ligand binding domain.