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Hormone resistant prostate cancer is a sign of advancing disease. Excluding cancers of the skin, cancer of the prostate is the second most common cause of cancer death in men. If prostate cancer is found early, before it metastasizes (spreads) beyond the prostate, there are four main treatment options:
- Radical prostatectomy (surgical removal of the prostate and affected surrounding tissue)
- Androgen deprivation therapy (ADT methods decrease testosterone production; aka hormone deprivation therapy)
- Radiation (carefully directed so that it kills the cancerous tissue)
- Surveillance (In “active surveillance” the cancer is closely monitored and treatment is begun if there is evidence of advancement. In “watchful waiting” there is no extra monitoring and only palliative measures are used (i.e., bothersome symptoms are addressed, but no attempts to cure the cancer are made).
The testicles produce 90% to 95% of a man’s testosterone. It is testosterone that causes prostate cancer to grow and spread. There are two methods of ADT. One is surgical removal of the testes (a procedure called orchiectomy). The other is the use of hormones that act on the testes to decrease testosterone production. In successful ADT (also called castration), the testosterone level is reduced to less than 50 ng/dL. The low hormone level slows prostate cancer’s advance. However, some testosterone continues to be produced elsewhere in the body.
Hormone resistant prostate cancer develops in 20% to 30% of castrated patients following ADT. Doctors are alerted to the development of possible hormone resistant prostate cancer by increasing prostate specific antigen (PSA) levels, and/or by X-ray computed tomography (CT) and/or bone scans showing cancer spread. Doctors are also alerted by patient reports of bone pain or difficulty urinating.
How hormone resistant prostate cancer occurs
There are several theories to explain how hormone resistant prostate cancer occurs. One involves an increase in the number of testosterone action sites (called testosterone receptors) and/or an increase in the testosterone receptor’s sensitivity to testosterone. By increasing the number and/or sensitivity of the receptors, testosterone’s cancer promoting effects are maintained even though its amount is severely decreased.
Another method involves the immune system. Cancer cells cause inflammation. Over time, chronic inflammation decreases the ability of the body’s immune system to identify and attack cancer cells. Inflammation may also increase the sensitivity of testosterone receptors.
Read more in our Prostate Cancer Health Center.
Fong MK et al. A new era for castrate resistant prostate cancer: A treatment review and update. Journal of Oncology Pharmacy Practice 2012; 18(3): 343-54.
Kantoff RW et al. 2010. Sipuleucel-T Immunotherapy for castration resistant prostate cancer. The New England Journal of Medicine 2010; 365(5): 411-22.
Chodak GW. Medscape Reference: Drugs, Diseases, and Procedures: Prostate Cancer. Last update 4/23/13.
Hotte SJ, Saad F. 2010. Current management of castrate-resistant prostate cancer. Current Oncology. 17(Suppl 2): S72–S79.