As noted in chapter 1, men are also susceptible to breast cancer, and it can be just as deadly. The disease follows a similar course, but since men are often unaware that they can get breast cancer they may delay seeing a doctor when they find a suspicious lump, and therefore may be diagnosed too late for effective treatment.
Age is the greatest risk factor for developing breast cancer, but tumors in post-menopausal women are sometimes less aggressive than in those who are pre-menopausal.
A role for female sex hormones in breast cancer has long been suspected because women are far more susceptible than men. Early menarche and late menopause, which lengthen the period of exposure to sex hormones, increase the risk for breast cancer. The age at which a woman has her first child, the number of pregnancies, and whether she breast feeds may also be risk factors and are related to hormonal status. The amount of breast tissue available may be a factor, but small-breasted women are at similar risk to those with large breasts.
Many breast cancers are sensitive to female sex hormones such as estrogen and progesterone. Estrogen and possibly progesterone may stimulate breast cancers that have already begun to grow (promoter effects) rather than cause the disease. It used to be thought that estrogen and progesterone bind to specific receptors on the surface of the malignant cells, then enter the cells and provide biochemical signals that stimulate them to proliferate. In recent years, researchers have discovered that there are two types of estrogen receptors. The "classical" estrogen receptor is now designated alpha, and another receptor, discovered in 1995, is designated beta. Some tissues express both alpha and beta receptors. The beta receptor exists in all tissues that express alpha receptors but also in some tissues that do not. Estrogens can act on alpha and beta receptors independently or in combination, and can have either stimulatory or inhibitory effects on the cells depending upon the specific receptor that is bound. In other words, estrogen may stimulate cells to proliferate or may prevent the proliferation. The effect of estrogen depends upon the form of the hormone and the receptor it binds to.
Drugs that bind the alpha or beta receptors can act as estrogen agonists (mimics) in some tissues and antagonists in others. The different properties of these receptors are the basis for a class of drugs called selective estrogen receptor modulators (SERMs). The drugs tamoxifen and raloxifene are compounds of that class, and are antagonists of estrogen in breast tissue. They are sometimes called anti-estrogens.
The effect of progesterone is also mediated by different receptors (PR-A and PR-B) and is influenced by the presence or absence of estrogen. Progesterone by itself inhibits the growth of breast cancer cells studied in the laboratory by inducing cell cycle arrest in G1. In the presence of estrogens, however, progesterone can stimulate growth by increasing sensitivity to estrogen or to other growth factors. Estrogen receptors increase the expression of progesterone receptors. In vivo, progesterone stimulates both the maturation and proliferation of breast epithelium and is known to regulate expression of many other growth-related genes. The effects of progesterone on breast epithelium are obviously complex. Its role in breast cancer is still being investigated.
Although some ethnic groups have higher rates of breast cancer than others, the biology of the disease is not necessarily different between the groups. The type of cells involved, the size and location at diagnosis, and the course of treatment are more likely to influence the course of disease and the eventual outcome. African-American women have a lower incidence of breast cancer than American white women, but have a higher rate of fatalities from the disease. This is likely due to socioeconomic factors leading to a delay in diagnosis until the disease has already spread.
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