How Hormone Therapy Fights Breast, Prostate and Ovarian Cancer

By

Sarah Lewis, PharmD

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Some cancers are stimulated to grow in response to certain hormones. Hormone therapy blocks the effects of these hormones, depriving cancer cells of the fuel they need to grow. Hormone therapy usually involves taking medications. Using specific drugs to block hormone production or interfere with its effect can slow or stop cancer growth and can shrink tumors in some cases. Another type of hormone therapy is to remove part or all of an organ that makes the hormones. Hormone therapy is a common treatment for prostate cancer and certain kinds of breast and ovarian cancers.

Hormone Therapy for Breast Cancer

Breast cancer can be hormone-receptor positive or hormone-receptor negative. If it is positive, the breast cancer has receptors for the hormones estrogen (ER+), progesterone (PR+), or both. Most breast cancers are hormone-receptor positive. About 25 to 30% are hormone-receptor negative. Compared to hormone-receptor negative ones, hormone-receptor positive tumors tend to grow slowly. They are also more common in women who have gone through menopause.

The main types of hormone therapy for breast cancer include:

  • Aromatase inhibitors lower estrogen levels by blocking aromatase. Aromatase is an enzyme in fat that converts other hormones into estrogen. These drugs do not prevent the ovaries from making estrogen. Because of this, they are only effective in postmenopausal women with ER+ breast cancer.

  • Estrogen-receptor downregulators (ERDs) occupy the estrogen receptor on breast cells, including cancer cells. This blocks estrogen from attaching to the receptor. ERDs can also reduce the number of estrogen receptors and change their shape. When a receptor doesn’t look the way it should, estrogen won’t be able to attach as easily.

  • Gonadatropin-releasing hormone agonists (GnRHs) shut down estrogen production in the ovaries. This means they are only effective in premenopausal women. Some literature uses the term luteinizing hormone-releasing hormone (LHRH) instead of GnRH.

  • Selective estrogen-receptor response modulators (SERMs) also attach and occupy estrogen receptors in the breast to block estrogen.

Sometimes, doctors recommend removing the ovaries (oophorectomy) to stop estrogen production for hormone-receptor positive breast cancer.

Hormone Therapy for Prostate Cancer

Male hormones—androgens—are necessary for prostate cancer to grow. Hormone therapy for prostate cancer deprives it of the hormones it needs to grow. This is also called androgen deprivation therapy and androgen suppression therapy. Surgically removing the testicles will take away the source of the androgen, testosterone. However, medicines can accomplish nearly the same effect and have largely replaced surgery.

The main types of hormone therapy for prostate cancer include:

  • Anti-androgens compete with testosterone to occupy receptors on prostate cells, including prostate cancer cells. This blocks testosterone’s effects on the cells.

  • CYP17 inhibitors block an enzyme the body uses to convert cholesterol into testosterone. This lowers testosterone production in the testicles and other tissues, such as the prostate.

  • Estrogens are female sex hormones. They counteract the effects of male hormones. Other types of hormone therapy have replaced the use of estrogens. Doctors may still suggest this therapy in some cases.

  • Gonadotropin-releasing hormone (GnRH) agonists bind to receptors on the pituitary gland. These synthetic drugs chemically resemble natural GnRH. Initially, this causes the pituitary to increase signals to the testicles to produce more testosterone. After 7 to 10 days, the continued presence of the drug on the receptor will actually decrease testosterone production to almost nothing.

  • GnRH antagonists also attach to pituitary receptors. However, they do not mimic natural GnRH. As a result, they do not cause an initial flare of testosterone production. This makes them safer for men with advanced prostate cancer.

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Medical Reviewers: William C. Lloyd III, MD, FACS Last Review Date: Aug 28, 2017

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