Antihormone therapy is a type of hormone therapy that suppresses selected hormones or their effects, in contrast with hormone replacement therapy, which encourages hormone activity.
| Antihormone therapy | |
|---|---|
| Specialty | Endocrinology |
The suppression of certain hormones can benefit patients with certain cancers because certain hormones prompt or help the growth of a tumor.[1] This is especially true in cancers relating to the sex organs.[2]
Hormones are made by glands and circulated through the bloodstream.[3] Hormones may act as a signal to cells to grow by attaching to them.[3] Antihormone therapy blocks hormones from sending these messages to cells. If a diagnostic test shows cancer in places with hormones attached, drugs may be prescribed to the patient to block the receptors and inhibit the growth of cancer cells.[3] Most antihormone therapies are administered by pill for 5 to 10 years after surgery.[4]
Origin
editHormone replacement therapy began in the 1960s but gained traction in the late 1990s.[5] Therapy methods have been developed rapidly since the 1970s, and survivorship of individuals with hormone receptor-positive cancer has skyrocketed.[6] In more recent years, since the 1990s, new classes of drugs have been released and greatly changed the way hormonal cancers, like prostate and breast cancer, are treated.[7] Research to understand how hormones influence the growth of cancer cells has prompted researchers to find new ways to use drugs to prevent and treat hormone receptor-positive cancer cells by limiting the production of sex hormones.[7] These methods of hormone suppression have opened the door for pioneering new cancer chemoprevention drugs.[7]
Types of Antihormone Therapy
editSERMs (selective estrogen receptor modulator) and SERDs (selective estrogen receptor degrader)
editTamoxifen and Toremifene
editTamoxifen is a SERM and is one of the most common and oldest forms of hormone therapy.[8] When breast cancer is found at an early stage or found to be Metastatic breast cancer, tamoxifen can be prescribed to selectively block estrogen's effect on certain cells. SERMs like tamoxifen attach to receptors on the cancer cells which blocks estrogen from attaching to the receptors. Tamoxifen is successful in lowering breast cancer reoccurrence rates, breast cancer occurrence in the opposite breast, and death from breast cancer in cases of hormone receptor-positive and hormone-sensitive cancer.[9] Tamoxifen is also thought to lower the risk of breast cancer in those who have a predisposition or at risk.[9] Tamoxifen may be used in pre and postmenopausal women.[10] Toremifene is a similar SERM drug to tamoxifen, but is less common and only approved for treatment of metastatic cancer. Toremifene is generally prescribed once tamoxifen is no longer effective.[11]
Fulvestrant (Faslodex)
editFulvestrant is a SERD drug that acts by damaging and blocking estrogen receptors.[11] Fulvestrant is currently only approved by the FDA to treat cancer in postmenopausal women, but it is often prescribed off-label in combination with and LHRH agonist in premenopausal women to halt the functionality of the ovaries.[11] Fulvestrant is administered via injection in the buttocks.[11]
Aromatase inhibitors
editA group of drugs called aromatase inhibitors are commonly prescribed to postmenopausal women who test positive for hormone receptor-positive cancer. Aromatase in fat and muscle can circulate estrogen in postmenopausal women.[12] Aromatase in highly estrogen-sensitive tissues, such as the breast, uterus, vagina, bone, and blood vessels, provides estrogen locally, so aromatase inhibitors work by reducing this estrogen production.[12]
Ovarian Suppression
editOvarian suppression is known to slow the growth of hormone receptor-positive breast cancer in premenopausal women[13] and can also help preserve fertility during chemotherapy.[14] Ovarian suppression through drugs temporarily shuts down the ovaries preventing the production of oestrogen, thus slowing the rate of growth of hormone receptor-positive tumors.[14] Ovary suppression may also be achieved through surgical intervention known as an oophorectomy, which removes one or both ovaries sometimes in combination with the fallopian tubes.[15]
LHRH Agonist
editLHRH (luteinising hormone-releasing hormone) agonists block the production of sex hormones in both men and women.[16] In men, LHRH agonists seize testosterone production in the testicles, and in women it blocks the ovaries from producing estrogen and progesterone.[16] These drugs are most commonly used in treatments for prostate cancer.[16]
Side Effects
editSide effects of antihormone therapy are generally minimal, but can produce similar feelings to menopause in women.[4] Common symptoms of all antihormone therapies include irregular menstrual cycles, hot flashes, weight gain, vaginal dryness, headaches, mood swings and hair thinning.[4] Less common but more serious drug-specific side effects include:[11]
SERMs
edit- Blood clots
- Stroke
- Cataracts
- Uterine cancer
- Decreased libido
- Mood swings and depression
Ovarian suppression
edit- Osteoporosis
- Decreased libido
- Mood swings and depression
Aromatase Inhibitors
editFulvestrant
edit- Gastrointestinal complications (nausea, vomiting, constipation)
- Bone and musculoskeletal pain
- Headache
References
edit- ^ "Definition of antihormone therapy - NCI Dictionary of Cancer Terms". Archived from the original on October 16, 2007.
- ^ Parczyk, Karsten and Martin R. Schneider. The future of antihormone therapy: innovations based on an established principle. Experimental Oncology. 14 December 1995 . 6 Jun 2008.
- ^ a b c "Breast Cancer Anti-Hormone Therapy | OSUCCC – James". The James - OSUCCC. Retrieved 2021-04-21.
- ^ a b c "Anti-Hormonal Therapies - UCLA Breast Health". www.uclahealth.org. Retrieved 2021-04-22.
- ^ Cagnacci, Angelo; Venier, Martina (2019-09-18). "The Controversial History of Hormone Replacement Therapy". Medicina. 55 (9): 602. doi:10.3390/medicina55090602. ISSN 1010-660X. PMC 6780820. PMID 31540401.
- ^ Jordan, V. Craig; Obiorah, Ifeyinwa; Fan, Ping; Kim, Helen R.; Ariazi, Eric; Cunliffe, Heather; Brauch, Hiltrud (October 2011). "Evolution of Long-Term Adjuvant Anti-hormone Therapy: Consequences and Opportunities. The St. Gallen Prize Lecture". Breast (Edinburgh, Scotland). 20 (Suppl 3): S1–11. doi:10.1016/S0960-9776(11)70287-9. ISSN 0960-9776. PMC 3521565. PMID 22015273.
- ^ a b c "Evolution of Cancer Treatments: Hormone Therapy | American Cancer Society". www.cancer.org. Retrieved 2021-04-22.
- ^ "Tamoxifen: Drug Information". Breastcancer.org. 2020-05-06. Retrieved 2021-04-22.
- ^ a b "Tamoxifen for Breast Cancer Treatment". Susan G. Komen®. Retrieved 2021-04-22.
- ^ "Hormone Therapies for Breast Cancer Treatment". Susan G. Komen®. Retrieved 2021-04-22.
- ^ a b c d e "Hormone Therapy for Breast Cancer | American Cancer Society". www.cancer.org. Retrieved 2021-04-22.
- ^ a b Fabian, C J (December 2007). "The what, why and how of aromatase inhibitors: hormonal agents for treatment and prevention of breast cancer". International Journal of Clinical Practice. 61 (12): 2051–2063. doi:10.1111/j.1742-1241.2007.01587.x. ISSN 1368-5031. PMC 2228389. PMID 17892469.
- ^ "Ovarian Suppression Therapies for Breast Cancer Treatment". Susan G. Komen®. Retrieved 2021-04-22.
- ^ a b "Ovarian suppression". Breast Cancer Now. 2015-06-08. Retrieved 2021-04-22.
- ^ "Oophorectomy". Cleveland Clinic. Retrieved 2021-04-22.
- ^ a b c "LHRH agonist". National Cancer Institute Dictionary of Cancer Terms. Archived from the original on 2021-03-24. Retrieved 2021-04-22.