Estrogen Receptors and Breast Cancer
Breast tissue contains estrogen receptors. During each menstrual cycle, estrogen triggers the proliferation of cells that form the inner lining of the milk glands in the breast, thereby preparing the breast to produce milk if the woman should become pregnant. If pregnancy does not occur, estrogen levels fall dramatically at the end of each monthly menstrual cycle. In the absence of high estrogen levels, those milk gland cells that have proliferated in any given month will deteriorate and die, followed by a similar cycle of cell proliferation and cell death the following month. For the average woman, this means hundreds of cycles of breast cell division and cell death repeated over a span of roughly 40 years, from puberty to menopause.
Although the proliferation of cells in the breast is a normal human process, estrogen can be harmful. Specifically, the proliferation of cells in the breast can increase a woman's chance of developing breast cancer.
Breast cancer is caused by DNA damage (i.e., mutations) in genes that regulate cell growth and division. Some mutations are inherited, while others are caused by exposure to radiation or to mutation-inducing chemicals such as those found in cigarette smoke. Mutations also can occur spontaneously as a result of mistakes that are made when a cell duplicates its DNA molecules prior to cell division.
Estrogen stimulates cell proliferation and, therefore, if one or more breast cells already possesses a DNA mutation, that increases the risk of developing breast cancer, these cells will proliferate (along with normal breast cells) in response to estrogen stimulation. The result will be an increase in the total number of mutant cells, any of which might thereafter acquire the additional mutations that lead to uncontrolled proliferation and the onset of cancer. In other words, estrogen-induced cell production leads to an increase in the total number of mutant cells that exist. These cells are at increased risk of becoming cancerous, so the chances that cancer may actually develop are increased.
Even in women who do not have any mutant breast cells, estrogen-induced proliferation of normal breast cells may increase the risk of developing breast cancer. The reason involves DNA. A cell must duplicate its DNA molecules prior to each cell division, thereby ensuring that the two new cells resulting from the process of cell division each receive one complete set of DNA molecules. But the process of DNA duplication occasionally makes mistakes, so the resulting DNA copies may contain a small number of errors (i.e., mutations). If one of these spontaneous mutations occurs in a gene that controls cell growth and division, it could lead to the development of cancer.
If you are diagnosed with breast cancer, your cancer cells will be tested to determine whether estrogen causes those cancer cells to grow. Unlike normal breast cells, cancer cells in the breast do not always have receptors for estrogen. Breast cancers that have estrogen receptors are said to be "estrogen receptor-positive" (ER+); breast cancers that do not possess estrogen receptors are "estrogen receptor-negative" (ER-).
Since estrogen promotes the development of cancer in the breast, in ER+ tumors, scientists postulated that substances that block the action of estrogen might be helpful in preventing or treating this type of cancer. Scientists thus developed "antiestrogen" drugs that can block the action of estrogens and thereby interfere with, or even prevent, the proliferation of breast cancer cells. Antiestrogens work by binding to estrogen receptors, blocking estrogen from binding to these receptors.
The first drug to be developed for its anticancer properties was Tamoxifen. Tamoxifen blocks the action of estrogen in breast tissue. Tamoxifen exerts this antiestrogenic effect by binding to the estrogen receptors of breast cells, thereby preventing estrogen molecules from binding to these receptors. As a result, the genes that stimulate cell proliferation cannot be activated. By interfering with estrogen receptors in this way, Tamoxifen blocks the ability of estrogen to stimulate the proliferation of breast cells.
The first step in treating women with breast cancer is breast cancer surgery. Studies show that when Tamoxifen is used after surgery, the risk of cancer recurrence is reduced. The growth of estrogen receptor-negative (ER-) cancer cells is not governed by estrogen, and is not treated with Tamoxifen.
Studies have also shown that Tamoxifen prevents women who are at high risk of getting breast cancer from getting breast cancer at all.
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