Breast cancer is the most common cancer among women, representing 32% of the cancers in women. One in eight women in their lifetime will develop breast cancer. In the U.S. there are 180,000 new cases of breast cancer annually. Fortunately the five-year survival rate is 86%. But unfortunately breast cancer is becoming more common. One in fourteen women developed breast cancer in 1960. Between 1950 and 1987 the incidence of breast cancer rose approximately 1% per year. It might be secondary to a longer lifespan or it may be secondary to using synthetic hormones. See chapter on estrogen. Increasing age is the greatest risk factor for breast cancer. Other risks include smoking, obesity, alcohol, a strong family history, not giving birth or giving birth late in life, and lack of breastfeeding. 80% of women with breast cancer have none of these risks. Most benign growths, such fibroadenomas, do not increase the risk of breast cancer.
Breast tissue cells are very responsive to estrogen and progesterone. Estrogen causes breast cells to proliferate, whereas progesterone counterbalances the aggressive effects of estrogen. Many breast cancers have estrogen receptors. It is believed that these cancerous cells will grow more rapidly if estrogen is in the body. A recent study showed that women on bioidentical hormonesafter breast cancer diagnosis had a 50% lower recurrence rate. Indole-3-carbinol (I3C), derived from broccoli, inhibits the growth and proliferation of breast cancer cells. Aspirin has been shown to decrease the risk of breast cancer by 30% because of its anti-inflammatory action.
The biggest fear that women have when taking estrogen is the possibility of developing breast cancer. Among women surveyed, 40% felt that the leading cause of death in women is breast cancer, when in reality it is 4%. Whether or not estrogen causes breast cancer is still not known. Prior to the WHI study there were more than fifty case control and cohort studies with mixed findings, thus the findings have been inconclusive. If there is an increased risk, the risk must be small. See the chapter on research on hormone replacement therapy. The largest cohort study retrospectively looked at 46,355 women who were evaluated for 15 years in the Breast Cancer Demonstration Project. There were 2082 incidents of breast cancer. Women taking estrogen alone had a 1.2 fold increase in breast cancer, whereas women taking estrogen and a progestin had a 1.4fold increase in breast cancer. These risks are shown to decrease after stopping HRT, and are almost nonexistent five years after stopping. These studies only looked at synthetic hormones, so the hormones a woman naturally produces have not been properly evaluated. Synthetic estrogens have been shown to increase density and mitotic activity in breast tissue. Synthetic estrogens are not only foreign to the body, but many are more aggressive than bioidentical estrogens. The use of synthetic estrogens, including birth control pills, could account for the recent increase in breast cancer.
Progesterone is cancer protective. Progesterone reduces the mitotic change in endometrial and breast tissue. It reduces cell proliferation and it enhances natural killer cells, interleukin-2, and the p53 molecule. Natural killer cells and interleukin-2 are important components of the immune system. Molecule p53 coordinates the actions of more than 60 genes that prevent damaged cells from turning cancerous. Progesterone increases apoptosis (cell destruction) before damaged cells convert to malignancies. Several studies have shown that the higher a woman’s progesterone, the less likely she is of developing cancer. Synthetic progestins have been shown to increase the incidence of breast cancer. The recent increase in breast cancer could very well be secondary to the lack of progesterone. Progesterone becomes deficient in a woman’s forties and it is completely absent by menopause. Women continue to produce some estrogen and they often take synthetic estrogens and progestins. There is strong evidence that this causes the breast to become estrogen dominant. Unless natural progesterone is in her body, she is most likely increasing her risk of breast cancer.
Studies have shown that women who take HRT have a greater chance of surviving breast cancer. The breast cancer in women who use HRT are more localized, lower grade, smaller tumors, and more likely to be lobular in origin. Ductal carcinomas of the breast are more ominous than lobular carcinomas. As a result there is a 40-60% reduction in mortality when compared with women who developed breast cancer without a history of HRT.
Studies on bioidentical hormones are limited regarding breast cancer. Estriol has been postulated to be protective but doctors are not using it so studies will continue to be limited. Every baby a woman has lowers her chance of breast cancer by 7%. This is ironic because when a woman is pregnant she is exposed to more than ten times the amount of estrogen and progesterone than any other time in her life. It very well could be the high levels of estriol during pregnancy that is responsible for this protection. Early pregnancies are protective against breast cancer not only because of the early exposure to estriol, but also because the p53 gene is upregulated in early pregnancies.
Breast cancer can occur secondary to an inherited gene mutation. BRCAI and BRCAII gene abnormalities have been shown to increase the risk of both ovarian and breast cancer. BRCAI and BRCAII are tumor suppressor genes that have a particular importance in breast and ovarian cells. The general risk for carrying a mutation in either BRCA genes is between 1 in 400 and 1 in 800. Jewish women of Eastern European decent have a 1 in 40 risk of a BRCA gene mutation. If an inherited mutation in the gene is discovered, women have an 87% lifetime risk of developing breast cancer. If there is a strong family history of breast and/or ovarian cancer BRCA testing should be performed. It is a blood test and the test is very expensive. If the test is positive, women should be counseled concerning their options.
There are many different treatment protocols for breast cancer. Options change with the type of cancer, nodal involvement, and the estrogen receptor status of the tumor. The decision should be made by the patient with input from the surgeon and the oncologist. Treatment usually consists of a combination of two or more of the following: mastectomy, lumpectomy, axillary node dissection, radiation, and/or chemotherapy. After this, five years of Tamoxifen is usually recommended; see the chapter on SERMs. Tamoxifen works by binding to estrogen receptors within the breast, preventing estrogen from binding to those receptors. After five years, the estrogen receptors become resistant to Tamoxifen, and it is no longer effective. A new drug called Femara is now being used after Tamoxifen. Femara is an aromatase inhibitor that works by decreasing the amount of estrogen production in the body. Studies have shown that Femara decreases the recurrence of breast cancer by 43%. Other aromatase inhibitors are Aromasin and Arimidex.
Mammography is the best screening test for the detection of breast cancer. A mammogram is an X-ray of the breasts. Despite what you have seen in the news, there is no controversy with screening mammography. Early detection of cancer is crucial, because the quicker a cancer is diagnosed, the better the survivability. The five-year survival rate for breast cancers detected and treated at an early stage is 95%. Women should get annual mammograms starting at age 40. The controversy with mammography stems from the exposure to radiation secondary to the procedure. Radiation can cause cells to become damaged, which can ultimately lead to cancer. We are unfortunately exposed to radiation daily.
A woman gets just as much radiation from flying across the country as she gets from a mammogram. The newer mammography machines not only are able to identify smaller lesions but they also give the patient less radiation. The main problem with mammography is false-positive findings. Not only does this give women anxiety, but it leads to further tests such as spot compressions, ultrasounds, and breast biopsies. Women under the age of 50 have denser breast tissue secondary to estrogen exposure. Denser breasts are more difficult to evaluate with mammography so there are more false-positive readings in younger women.
Women who are at high risk for developing beast cancer should also get an MRI of their breasts. MRIs are ten times more costly than a mammogram but they are more accurate at detecting cancers. Unfortunately they have more false-positive findings, so more unnecessary biopsies are performed. If a woman or her physician is able to palpate a lesion, an ultrasound should be ordered. For palpable lesions, this is the best test. It can determine if the mass is solid or cystic. The problem with routine screening breast ultrasounds is that there are too many false-positive findings leading to unnecessary biopsies. Thermography is another widely used screening test.
Thermography detects heat within the breast. When there is a cancerous growth, the cancer recruits new blood vessels; this new blood supply results in increased heat within the breast. The problem with this test is that by the time there is a positive thermography reading, the cancer is usually quite large. Thermography cannot pick up early cancers, like ductal carcinoma in situ, whereas mammography is able to detect these early cancers. There are a lot of false-positive findings with thermography as well. False-positive findings lead to more extensive workups. Monthly selfbreast exams are the most important preventative measure against fatal breast cancer. More breast cancers are discovered by selfbreast exams than mammography and physicians combined.