Hormone-Receptor Assay
One vitally important laboratory test is the estrogen receptor (ER) "assay". Almost all pathologists do this test routinely on breast cancers. Measuring the number of receptors for the female hormone estrogen in a tumor's cells is an indirect way of learning whether or not the breast cancer depends on the hormone to grow. In addition, a second important marker- the receptor for progesterone (PR) - is usually included in the tests.
If most of the cells contain many receptors, the tumor is "ER-rich" or "positive". A tumor whose cells contain few receptors is "ER-poor" or "negative". Although the words "positive" and "negative" are used to describe the results of an ER assay. The important question is how many estrogen receptors are in a specific volume of cellular material.
Women whose breast cancers are "fed" by estrogen (are ER-positive) may be helped by having the female hormone's action blocked by antiestrogens, like the drug "tamoxifen", that "starve" microscopic tumor cells left behind after surgery. Precisely how tamoxifen acts against breast cancer is still being studied, but scientists know it is a "cytostatic" drug: it prevents tumor cells from dividing but doesn't kill them.
Normally, molecules of estrogen in a woman's blood enter breast cancer cells and are attracted (bind) to the receptors just as bits of iron are attracted to a magnet. Tamoxifen mimics estrogen so well, molecules of the antiestrogen act like a "Trojan Horse" by binding to the cells receptors. Real estrogen in the bloodstream then has no empty "binding sites" in the cancer cells to attach to and cannot stimulate the tumor to grow.
When progesterone receptors (PR) are also present, their level is important in helping predict response to hormonal therapy.

Hormone replacement therapy

The use of hormone replacement therapy (HRT) poses a dilemma for the rising numbers of breast cancer survivors, many of who enter menopause prematurely as a result of therapy. HRT has generally not been used for women with a history of breast cancer because estrogen is a growth factor for most breast cancer cells in the laboratory. Neither pregnancy after breast cancer nor the use of oral contraceptive pills before a diagnosis of breast cancer has been shown to adversely impact survival when controlled for stage of disease. Reports from small uncontrolled series of breast cancer survivors treated with low-dose HRT did not show adverse impact upon survival These findings provide the rationale for prospective clinical trials testing the safety of HRT for women with a history of breast cancer.