Breast cancer is a treatable and curable disease. Early detection is the key to a cure. The cancer usually starts as a small lump. However, with time the lump may grow and spread to nearby areas, such as the skin or the lymph nodes under the arm. Later, the tumor may spread to vital organs such as the liver, brain, lungs, and bones. If breast cancer is found early, before it spreads, it can be cured.Keep a healthy weight. Women who gain 20 to 30 pounds after their teens are more likely to get breast cancer than those who don't gain this much weight. This is because fat cells produce estrogen, which promotes breast cancer.

In most cases, doctors don't know what causes breast cancer. The number of tumors associated with a mutation in the breast cancer gene is small — about 10 percent to 15 percent. That's why research is focusing on newer measures you can take that may help reduce your risk.

As with many medical conditions, the caloric imbalance that results in obesity often develops from a combination of genetic and environmental factors. Polymorphisms in various genes controlling appetite, metabolism, and adipokine release predispose to obesity, but the condition requires availability of sufficient calories, and possibly other factors, to develop fully. Various genetic abnormalities that predispose to obesity have been identified (such as Prader-Willi syndrome and leptin receptor mutations), but known single-locus mutations have been found in only about 5% of obese individuals. While it is thought that a large proportion of the causative genes are still to be identified, much obesity is likely the result of interactions between multiple genes, and non-genetic factors are likely also important.

Hormones may relieve menopausal symptoms, but women and their healthcare providers should weigh the potential risks of therapy against the potential benefits for menopausal symptom control.The National Institutes of Health has stopped the estrogen-only phase of the Women’s Health Initiative (WHI) after finding an increased risk of stroke and no reduction in the risk of heart disease in postmenopausal women who have had a hysterectomy. Previously, in 2002, the combination of estrogen-plus-progestin arm of WHI was stopped early because of an increase in breast cancer in patients on active medication. That arm of the study also found no reduction, but rather an increase in heart disease and stroke.

Although taking hormone therapy is not useful to prevent heart disease, these guidelines provide many other proven methods of lowering a woman’s risk, such as stopping smoking, controlling blood pressure and cholesterol levels, staying physically active and lean, and adding medications with a demonstrated benefit in women who are at specific levels of personal risk for heart disease or stroke.

Women's Health Initiative study of 2002 raised concerns about the use of hormone therapy for symptoms of menopause. Among other problems, long-term treatment with estrogen-progestin combinations such as those found in the drug Prempro increased the risk of breast cancer. If you're taking hormone therapy, consider your options with your doctor.

Some women have what is known as HER2-positive breast cancer. HER2, short for human epidermal growth factor receptor-2, is a gene that helps control cell growth, division, and repair. When cells have too many copies of this gene, cell growth speeds up. It’s believed that HER2 plays a key role in turning healthy cells into cancerous ones. Some women with breast cancer have too much HER2, and are therefore considered HER2-positive.

Hormone therapy is sometimes used to treat breast or prostate cancer. The hormone estrogen can make breast cancer tumors grow faster. Similarly, the hormone testosterone can make cancerous tumors in the prostate grow faster. Drugs that contain other hormones may be used to block the effects of estrogen and testosterone.

The radiologic appearance of the breast varies depending on the relative amounts of fat, connective tissue, and epithelial tissue. Breast tissue ranges from tissue made up entirely of fat to tissue occupied by diffuse or nodular densities. These variations in the density of breast tissue on mammography are referred to as the parenchymal pattern of the breast. Parenchymal density has been shown histologically to be inversely correlated with fat content and directly correlated with fibrous- and epithelial-tissue content.

Breast density decreases with increasing age, postmenopausal status, increasing number of births, and declining body weight, suggesting that the tissue changes responsible for breast density are under hormonal control. Furthermore, women who have dense breasts on mammography have higher serum estrogen concentrations than women with less dense breasts, and estrogen-replacement therapy increases breast density in postmenopausal women.Several studies of women with family histories of breast cancer, increased breast density on mammography was more common than expected,88,89 suggesting that it may be genetically determined, at least in part,90 but this association has not been confirmed by other studies.

Italian researchers are shedding light on how leptin, a hormone found in fat cells, may play a major role in the development and progression of breast cancer.

The research, presented at the Experimental Biology meeting in Washington, D.C., identifies a new mechanism for the link between obesity and breast cancer and suggests new targets for drugs to interfere with that mechanism, said researcher Dr. Sebastiano Ando.

He noted that obesity increases the risk of breast cancer in postmenopausal women, shortens the time between cancer recurrence, and lowers overall survival rates. In a previous study, Ando's team found that leptin increases the amount of estradiol (a type of estrogen) in breast tissue.

This new study found that combined exposure to leptin and estradiol increased the size of breast cancer tumors in both mice and in tissue cultures. This growth in tumor size was accompanied by an increase in E-cadherin, an intracellular adhesion molecule generally regarded as a tumor suppressor.

But the researchers said their findings suggest that E-cadherin may act as a tumor enhancer when it's exposed to leptin and estradiol. In that case, E-cadherin's ability to help cells gather together enhances the transformation of normal cells to cancerous cells, thus stimulating tumor growth.

Ando and his colleagues found that this increased cell growth was halted when they used an E-cadherin antibody or a calcium-chelating agent to block E-cadherin function in the presence of estradiol.