A 50-year-old man with prostate cancer on androgen deprivation therapy with goserelin (GnRH agonist) and bicalutamide (anti-androgen) develops resistance after 18 months. His PSA rises despite castrate testosterone levels. The term for this clinical state and its underlying mechanism is:

• A Castration-resistant prostate cancer due to intratumoral androgen synthesis and AR amplification ✓
• B Anti-androgen withdrawal syndrome due to AR mutation making bicalutamide an agonist
• C GnRH agonist resistance due to receptor downregulation failure
• D Androgen insensitivity syndrome due to AR gene deletion

Explanation

Castration-resistant prostate cancer (CRPC) is defined by rising PSA despite castrate testosterone levels (<50 ng/dL). Mechanisms include intratumoral androgen synthesis, AR gene amplification/mutation, and AR splice variants. Anti-androgen withdrawal syndrome (option B) is a separate phenomenon where stopping bicalutamide paradoxically improves symptoms due to AR mutations that convert antagonists to agonists. CRPC is the more common progression pattern.

Reference: Katzung Basic and Clinical Pharmacology, 15th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.