Hormonal Therapy for Breast Cancer
Estrogen is an essential female hormone that is produced by the ovaries and adrenal glands. It serves many critical functions in the body, including developing the female sex organs in puberty, preparing the breasts and uterus for pregnancy in adulthood, and maintaining cardiovascular and bone health. Without estrogen, the female body is unable to sustain pregnancy and is susceptible to heart disease and osteoporosis.
Estrogen can also cause some cancers to grow. The breasts, uterus and other female organs are composed of cells that contain estrogen receptors. When cells that have estrogen receptors become cancerous, exposure to estrogen increases the cancer’s growth. Cancer cells that have estrogen receptors are referred to as estrogen receptor-positive (ER-positive) cancers.
The growth of ER-positive breast cancer cells can be prevented or slowed by reducing the exposure to estrogen. This is the goal of hormonal therapy for breast cancer. However, a reduction in estrogen levels can also result in side effects because estrogen is necessary for important body functions, such as bone growth and cardiovascular health. Lower estrogen levels lead to decreased bone density and heart disease.
Tamoxifen is an anti-estrogen drug that has historically been a mainstay of hormonal therapy. However, several newer hormonal therapy drugs, referred to as aromatase inhibitors, have been shown to improve outcomes among postmenopausal patients with ER-positive breast cancer.
- How Does Hormonal Therapy Work?
- What Are the Side Effects of Hormonal Therapy?
- How Are Hormonal Therapies Used in the Treatment of Early-stage Breast Cancers?
- How Are Hormonal Therapies Used in the Treatment of Metastatic or Recurrent Breast Cancer?
- Can Hormonal Therapy Reduce the Risk of Developing Breast Cancer?
- Are There Other Benefits Associated with hormonal Therapy?
- What New Strategies Are Being Developed to Improve the Hormonal Therapy?
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How Does Hormonal Therapy Work?
In premenopausal women, the ovaries are the major source of estrogen. After menopause, when ovarian hormone production drops dramatically, some estrogen continues to be produced in tissues outside of the ovaries. In this process, androgens produced by the adrenal glands are converted into estrogen. An enzyme called aromatase is required for this conversion.
The goal of hormonal therapy is to decrease the effect of estrogen on cancer cells. Reducing the effects of estrogen can be accomplished in the following ways:
- by removing the ovaries, which produce the majority of estrogen in premenopausal women
- by blocking the conversion of androgens to estrogens by inhibiting the aromatase enzyme, or
- by blocking the estrogen receptors so that estrogen cannot bind and stimulate growth-related activity in breast and other cells.
Currently, the types (classes) of anti-estrogen drugs that are approved for the treatment of patients with breast cancer are called:
- Aromatase inhibitors
- Selective estrogen receptor modulators (SERMs)
- Estrogen receptor antagonists
These three classes of drugs work by decreasing estrogen’s effects on the body, but they do so through different mechanisms.
Aromatase inhibitors: Aromatase inhibitors block the conversion of androgens to estrogen, and reduce estrogen levels in postmenopausal women. Currently, three anti-aromatase drugs are approved for the treatment of postmenopausal women with breast cancer: Femara® (letrozole) Arimidex® (anastrozole), and Aromasin® (exemestane).,, Femara and Arimidex are nonsteroidal aromatase inhibitors that bind reversibly to aromatase. Aromasin is a steroidal aromatase inhibitor that binds permanently to aromatase.
Selective Estrogen Receptor Modulators (SERM): SERMs block estrogen receptors within breast cells, thereby reducing estrogen-stimulated growth. Currently, tamoxifen is the most common SERM used for the hormonal treatment of breast cancer. However, tamoxifen is associated with side effects, including an increased risk of uterine cancer.
Estrogen receptor antagonist: Like SERMs, estrogen receptor antagonists work by preventing estrogen from stimulating the growth of estrogen receptor-positive cells. Faslodex® (fulvestrant), the first estrogen receptor antagonist, binds to and degrades estrogen receptors so that estrogen is no longer able to bind to the receptors and stimulate cellular growth. The Food and Drug Administration (FDA) has approved Faslodex for hormone treatment in postmenopausal women with ER-positive breast cancer that has failed previous hormone therapies.