hormonal anticancer therapy
Hormonal anticancer therapy treats cancers that feed on the body's own hormones by cutting off that supply. Some tumours are like plants that grow only when watered: certain breast cancers depend on estrogen, and most prostate cancers depend on testosterone. If you stop the hormone, or block its receptor, the dependent tumour starves and shrinks.
There are two broad strategies. One blocks the hormone receptor directly, so the hormone can no longer deliver its growth signal; tamoxifen blocks the estrogen receptor in breast cancer, and antiandrogens block the androgen receptor in prostate cancer. The other lowers hormone levels: aromatase inhibitors cut estrogen production in postmenopausal women, and GnRH agonists or surgical removal of the gland reduce sex-hormone output. These approaches are forms of targeted treatment based on a tumour's hormone receptors.
Hormonal therapy is generally far gentler than cytotoxic chemotherapy, but it is not benign. Lowering or blocking sex hormones can cause hot flushes, bone thinning, mood and sexual effects, and tamoxifen carries a small risk of uterine cancer and clots. It also only helps hormone-receptor-positive tumours, and these cancers can eventually become resistant and grow despite hormone blockade.
Tamoxifen, taken for years after surgery for estrogen-receptor-positive breast cancer, blocks the estrogen receptor and substantially lowers the chance of the cancer returning.
Receptor blockade only helps hormone-receptor-positive tumours, and resistance can still develop over time.