Prostate cancer medical therapy: Difference between revisions
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:* [[Gonadotropin-releasing hormone analog|GnRH antagonists]] suppress the production of LH directly, while [[Gonadotropin-releasing hormone analog|GnRH agonists]] suppress LH through the process of [[downregulation]] after an initial stimulation effect. [[Abarelix]] is an example of a GnRH antagonist, while the GnRH agonists include [[leuprolide]], [[goserelin]], [[triptorelin]], and [[buserelin]]. Initially, GnRH agonists increase the production of LH. However, because the constant supply of the medication does not match the body's natural production rhythm, production of both LH and GnRH decreases after a few weeks.<ref>{{cite journal| last=Loblaw| first=DA| coauthors=Mendelson DS, Talcott JA, Virgo KS, Somerfield MR, Ben-Josef E, Middleton R, Porterfield H, Sharp SA, Smith TJ, Taplin ME, Vogelzang NJ, Wade JL Jr, Bennett CL, Scher HI; American Society of Clinical Oncology| title=American Society of Clinical Oncology recommendations for the initial hormonal management of androgen-sensitive metastatic, recurrent, or progressive prostate cancer| journal=J Clin Oncol| year=2004| month=July 15| volume=22| issue=14| pages=2927–41| pmid=15184404| doi=10.1200/JCO.2004.04.579}} Erratum in: J Clin Oncol. 2004 November 1;22(21):4435.</ref> | :* [[Gonadotropin-releasing hormone analog|GnRH antagonists]] suppress the production of LH directly, while [[Gonadotropin-releasing hormone analog|GnRH agonists]] suppress LH through the process of [[downregulation]] after an initial stimulation effect. [[Abarelix]] is an example of a GnRH antagonist, while the GnRH agonists include [[leuprolide]], [[goserelin]], [[triptorelin]], and [[buserelin]]. Initially, GnRH agonists increase the production of LH. However, because the constant supply of the medication does not match the body's natural production rhythm, production of both LH and GnRH decreases after a few weeks.<ref>{{cite journal| last=Loblaw| first=DA| coauthors=Mendelson DS, Talcott JA, Virgo KS, Somerfield MR, Ben-Josef E, Middleton R, Porterfield H, Sharp SA, Smith TJ, Taplin ME, Vogelzang NJ, Wade JL Jr, Bennett CL, Scher HI; American Society of Clinical Oncology| title=American Society of Clinical Oncology recommendations for the initial hormonal management of androgen-sensitive metastatic, recurrent, or progressive prostate cancer| journal=J Clin Oncol| year=2004| month=July 15| volume=22| issue=14| pages=2927–41| pmid=15184404| doi=10.1200/JCO.2004.04.579}} Erratum in: J Clin Oncol. 2004 November 1;22(21):4435.</ref> | ||
====Side effects of hormonal therapy=== | ====Side effects of hormonal therapy==== | ||
* [[Hot flush|hot flashes]] | * [[Hot flush|hot flashes]] | ||
* Weight gain | * Weight gain | ||
Revision as of 17:26, 18 September 2015
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Medical Therapy
Radiation therapy
- Radiotherapy uses ionizing radiation to kill prostate cancer cells. When absorbed in tissue, ionizing radiation such as Gamma and x-rays damage the DNA in cells, which increases the probability of apoptosis.
- Radiation therapy is commonly used in prostate cancer treatment
- It may be used instead of surgery or after surgery in early stage prostate cancer. Radiation therapy appears to cure small tumors that are confined to the prostate just about as well as surgery.
- In advanced stages of prostate cancer, radiation is used to treat painful bone metastases.
- Radiation therapy is often offered to men whose medical problems make surgery more risky.
- Two different kinds of radiation therapy are used in prostate cancer treatment:
Side effects of radiation therapy
- Both types of radiation therapy
Hormonal therapy
- Hormonal therapy uses medications or surgery to block prostate cancer cells from getting dihydrotestosterone (DHT), a hormone produced in the prostate and required for the growth and spread of most prostate cancer cells. Blocking DHT often causes prostate cancer to stop growing and even shrink.
- Hormonal therapy for prostate cancer targets the pathways the body uses to produce DHT. A feedback loop involving the testicles, the hypothalamus, and the pituitary, adrenal, and prostate glands controls the blood levels of DHT. First, low blood levels of DHT stimulate the hypothalamus to produce gonadotropin releasing hormone (GnRH). GnRH then stimulates the pituitary gland to produce luteinizing hormone (LH), and LH stimulates the testicles to produce testosterone. Finally, testosterone from the testicles and dehydroepiandrosterone from the adrenal glands stimulate the prostate to produce more DHT. Hormonal therapy can decrease levels of DHT by interrupting this pathway at any point.
- However, hormonal therapy rarely cures prostate cancer because cancers which initially respond to hormonal therapy typically become resistant after one to two years. Hormonal therapy is therefore usually used when cancer has spread from the prostate.
- It may also be given to certain men undergoing radiation therapy or surgery to help prevent return of their cancer.[3]
- There are several forms of hormonal therapy:
- Orchiectomy
- Antiandrogens
- GnRH antagonists suppress the production of LH directly, while GnRH agonists suppress LH through the process of downregulation after an initial stimulation effect. Abarelix is an example of a GnRH antagonist, while the GnRH agonists include leuprolide, goserelin, triptorelin, and buserelin. Initially, GnRH agonists increase the production of LH. However, because the constant supply of the medication does not match the body's natural production rhythm, production of both LH and GnRH decreases after a few weeks.[4]
Side effects of hormonal therapy
- hot flashes
- Weight gain
- Loss of libido
- Gynecomastia
- Osteoporosis
Chemotherapy
- Chemotherapy is used in the treatment of castrate resistant prostate cancer (also called hormone-refractory prostate cancer).
- The most commonly used regimen combines the chemotherapeutic drug liste below:
- Docetaxel with a
- Corticosteroid
Other Medications
- [[Bisphosphonates]
- Bisphosphonates such as zoledronic acid have been shown to delay skeletal complications such as fractures or the need for radiation therapy in patients with hormone-refractory metastatic prostate cancer.[6]
- Bone pain due to metastatic disease is treated with opioid. Pain relievers such as morphine and oxycodone
References
- ↑ Lawton, CA (1991). "Long-term treatment sequelae following external beam irradiation for adenocarcinoma of the prostate: analysis of RTOG studies 7506 and 7706". Int J Radiat Oncol Biol Phys. 21 (4): 935–9. PMID 1917622. Unknown parameter
|month=ignored (help); Unknown parameter|coauthors=ignored (help) - ↑ Brenner, DJ (2000). "Second malignancies in prostate carcinoma patients after radiotherapy compared with surgery". Cancer. 88 (2): 398–406. doi:10.1002/(SICI)1097-0142(20000115)88:2<398::AID-CNCR22>3.0.CO;2-V. PMID 10640974. Unknown parameter
|month=ignored (help); Unknown parameter|coauthors=ignored (help) - ↑ Robson, M (1996). "How is androgen-dependent metastatic prostate cancer best treated?". Hematol Oncol Clin North Am. 10 (3): 727–47. doi:10.1016/S0889-8588(05)70364-6. PMID 8773508. Unknown parameter
|month=ignored (help); Unknown parameter|coauthors=ignored (help) Review. - ↑ Loblaw, DA (2004). "American Society of Clinical Oncology recommendations for the initial hormonal management of androgen-sensitive metastatic, recurrent, or progressive prostate cancer". J Clin Oncol. 22 (14): 2927–41. doi:10.1200/JCO.2004.04.579. PMID 15184404. Unknown parameter
|month=ignored (help); Unknown parameter|coauthors=ignored (help) Erratum in: J Clin Oncol. 2004 November 1;22(21):4435. - ↑ Tannock, IF (2004). "Docetaxel plus prednisone or mitoxantrone plus prednisone for advanced prostate cancer". N Engl J Med. 351 (15): 1502–12. doi:10.1056/NEJMoa040720. PMID 1547021. Unknown parameter
|month=ignored (help); Unknown parameter|coauthors=ignored (help) - ↑ Saad F, Gleason DM, Murray R, Tchekmedyian S, Venner P, Lacombe L, Chin JL, Vinholes JJ, Goas JA, Chen B (2002). "A randomized, placebo-controlled trial of zoledronic acid in patients with hormone-refractory metastatic prostate carcinoma". J Natl Cancer Inst. 94 (19): 1458–68. PMID 12359855.