What Is Hormonal Therapy?

Hormonal therapy medicines are whole-body (systemic) treatment for hormone-receptor-positive breast cancers. Hormone receptors are like ears on breast cells that listen to signals from hormones. These signals "turn on" growth in cells that have receptors.

Most breast cancers are hormone-receptor-positive.

• About 80% of breast cancers are estrogen-receptor positive.
• About 65% of estrogen-receptor-positive breast cancers are also progesterone-receptor-positive.
• About 13% of breast cancers are estrogen-receptor-positive and progesterone-receptor-negative.
• About 2% of breast cancers are estrogen-receptor-negative and progesterone-receptor-positive.

If a cancer has receptors for either estrogen or progesterone, it's considered hormone-receptor-positive.

There are three different types of hormonal therapy medicines:

• aromatase inhibitors:
  • Arimidex (chemical name: anastrozole)
  • Aromasin (chemical name: exemestane)
  • Femara (chemical name: letrozole)
• SERMs (Selective Estrogen Receptor Modulators):
  • tamoxifen
  • Evista (chemical name: raloxifene)
  • Fareston (chemical name: toremifene)
• ERDs (Estrogen Receptor Downregulators):
  • Faslodex (chemical name: fulvestrant)

Hormonal therapy medicines can be used to:

• lower the risk of early-stage hormone-receptor-positive breast cancer coming back
• lower the risk of hormone-receptor-positive breast cancer in women who are at high risk but haven't been diagnosed with breast cancer
• help shrink or slow the growth of advanced-stage or metastatic hormone-receptor-positive breast cancers 

Hormonal therapy medicines treat hormone-receptor-positive breast cancers in two ways:

• by lowering the amount of the hormone estrogen in the body
• by blocking the action of estrogen in the body

Because it targets estrogen, hormonal therapy is also known as anti-estrogen therapy.

Estrogen has many different roles in your body, including keeping your bones strong and cholesterol low, as well as improving your sense of well-being. Before menopause, most of the estrogen in a woman's body is made by the ovaries. After menopause, the ovaries stop producing estrogen, but smaller amounts of estrogen are still made in the body; a steroid produced by the adrenal glands is made into estrogen in fat tissue.

After a breast cancer is removed, the cells are tested to see if they have receptors for two hormones: estrogen and progesterone. If a breast cancer is hormone-receptor-positive, it means that it has these hormone receptors, which act like ears or antennae. When estrogen in the body attaches to the receptors, the breast cancer cells respond to signals from the estrogen that tell the cells to grow and multiply. By reducing the amount of estrogen in the body or blocking the effects of estrogen, hormonal therapy medicines can slow the growth of or shrink advanced-stage/metastatic estrogen-receptor-positive breast cancers. Lowering the amount of estrogen or blocking its effects also can reduce the risk of an early-stage, estrogen-receptor-positive breast cancer coming back after surgery. Since hormonal therapy affects the action of estrogen but not progesterone in breast cancer cells, the value of hormonal therapy is less clear if your cancer is progesterone-receptor-positive and estrogen-receptor-negative. In this situation, you should discuss the value of hormonal therapy with your doctor.

In addition to taking a hormonal therapy medicine, pre-menopausal women diagnosed with hormone-receptor-positive breast cancer or who are at high risk for breast cancer also may want to consider temporary ovarian shutdown using medication or permanent ovarian shutdown by surgically removing the ovaries. The ovaries are the main source of estrogen before menopause, so ovarian shutdown or removal stops them from producing estrogen.

Hormonal therapy WON'T work on hormone-receptor-negative breast cancers. Hormone-receptor-negative breast cancers don't respond to estrogen, so reducing the amount of estrogen in the body doesn't affect hormone-receptor-negative cancers.