Breast Cancer


What should I know about Breast cancer?

The incidence of breast cancer has been increasing steadily for decades. In 1972 when President Nixon declared our national war on cancer, a woman’s lifetime risk of developing breast cancer was 1 in 20. Today breast cancer rates have escalated to the point where women’s lifetime risk of developing breast cancer is 1 in 8. In the year 2002, the American Cancer Society estimates that nearly 203,500 women will be diagnosed with breast cancer and approximately 39,600 women will die from the disease. This means that approximately every two and a half minutes a woman in the United States is diagnosed with breast cancer and that approximately every thirteen minutes, a woman dies from this disease. Breast cancer has become the second largest cause of cancer death in women, after skin cancer, and the leading cause of death for women between the ages of 35 and 54.

Malignant Breast Tumors
One of the most common ways to classify breast cancer is according to the type of cells where the cancer originates, such as the lobule, duct or connective tissue. Each breast has 15 to 20 sections called lobes and each contains many smaller sections called lobules. The lobes and lobules are connected by a network of thin tubes called ducts. Ductal cancer is the most common type of breast cancer, accounting for 85 to 90% of the cases. (1) Lobular cancer occurs in 10 to 12% of cases. Inflammatory breast cancer is an uncommon form of the disease, in which the breast becomes warm, red, swollen and inflamed.

Tumor Grade
Each type of breast cancer can be examined for its degree of "differentiation," which classifies the cancer according to how different its cells are from normal cells. This varies from well differentiated to poorly differentiated. Well differentiated cells are very similar to the cells of origin. On the other hand, poorly differentiated cells have bizarre appearances, retaining only a few characteristics of the original normal cells. This description of tumor differentiation is referred to as tumor "grade." Low-grade malignancies are well differentiated, while high-grade indicates poor differentiation. Determination of tumor grade is meaningful because this is highly related to the degree of aggressiveness of the cancers and to patient survival, with high-grade cancers usually carrying the worst prognoses.

Carcinoma In situ
Ductal breast malignancies are divided into two categories, pre-invasive which have not invaded surrounding tissues yet, and invasive. Pre-invasive ductal cancer is called intraductal carcinoma in situ (Latin for "in position"). This is a very early stage of breast cancer, which is so small that it can never be diagnosed on breast examination. Mammography is the only diagnostic method that can detect this in situ stage. In modern mammography centers, ductal carcinoma in situ (DCIS) composes 25% of all breast cancers detected by screening mammography. (2) In DCIS, the ductal cancer cells remain within the ducts, with no sign of outside tissue invasion. If DCIS is not treated surgically, it frequently evolves into invasive ductal carcinoma. (3) It is believed that all invasive ductal cancers began as non-invasive forms.

Lobular carcinoma in situ
Invasive lobular carcinomas only account for about 10% of all breast cancers and they tend to be somewhat less aggressive than invasive ductal carconomas. Unlike invasive ductal carcinomas, it is now believed that lobular carcinoma in situ (LCIS) is not a precursor of invasive lobular carcinoma. The confusion exists because LCIS, while it has the word carcinoma in its name, does not behave like a cancerous condition. It does not grow, form masses, transform into invasive cancer, or metastasize. Therefore, it does not represent a true malignancy. Also, LCIS cannot be diagnosed by a breast exam or mammogram. It is only diagnosed by accident when a breast biopsy is performed for another reason. LCIS represents a risk 7 to 12 times that of the general population for subsequent invasive cancer. (4)

Uncommon Breast Malignancies
Other types of breast malignancies occur less frequently. The first category is connective cancer breast cancers, which are referred to as breast sarcomas. Next are metastases, which are malignancies that have spread to the breast from a cancer in another part of the body. While spread of a cancer to other sites from the primary site is a common occurrence in many types of cancer, metastatic tumors rarely spread to the breasts from another primary site.

Metastasized Breast Cancer
Breast cancer is able to spread or metastasize to distant sites by two mechanisms; through the blood vessels or via the lymphatic ductal system. If a tumor invades the lymph ducts, it travels to the armpit (axilla) where the migrating tumor cells are caught in the filtering processes of the lymph nodes, which causes the nodes to enlarge. This can make the lymph nodes feel like firm lumps. From these initial nodes, cancer cells can continue to spread through this duct system to other parts of the body.

Clinical Staging
Clinical staging is another way to rate and compare disease activity. Each stage from 0 through IV represents an incremental worsening of the overall disease prognosis. Clinical staging is determined by considering the size of the tumor (T), the status of the nearby lymph nodes (N), and the existence of distance metastasis (M). (5)


Breast Health Global Initiative, 2004.

  • Breast cancer is the most prevalent cancer in the world today due to its high incidence and relatively good prognosis. An estimated 4.4 million women are alive today in whom breast cancer was diagnosed within the last five years.
  • However, breast cancer is the most common cause of cancer-related deaths among women worldwide.
  • More than 1.1 million women worldwide are newly diagnosed with breast cancer annually. This represents about 10% of all new cancer cases and 23% of all female cancers.
  • With more than 410,000 deaths each year, breast cancer accounts for about 14% of all female cancer deaths and 1.6% of all female deaths worldwide.
  • Incidence rates are climbing by as much as 5% annually in low-resource countries.


  • In 2003, there were 3738 female breast cancer cases that were reported, making it the most commonly diagnosed cancer in women.
  • It accounted for 31.0 % of newly diagnosed female cases.
  • Breast cancer was the commonest cancer in all ethnic groups and all age groups in females from the age of 15 years.
  • The overall Age Standardised Rate (ASR) was 46.2 per 100,000 population.

American Cancer Society Facts, 2000-2006.

An estimated 212,920 new cases of invasive breast cancer will be diagnosed in women during 2006. (6) In addition to invasive breast cancer, 61,980 new cases of breast carcinoma in situ are expected to occur among women during 2006. (7) An estimated 40,970 women will die from breast cancer in 2006. (8) Over 75% of women who are diagnosed with breast cancer are age 50 or older. Men can get breast cancer, although this is very rare. An estimated 1,720 new cases will be diagnosed in men during 2006. An estimated 460 men will die from breast cancer in 2006. About 5-10% of all breast cancers are inherited. Children can inherit an altered breast cancer susceptibility gene from either their mother or father. Most women—about 80%—who get breast cancer do not have a sister or mother who has breast cancer. Excluding skin cancer, breast cancer is the most common cancer in women. Although the lifetime risk of breast cancer is 1 in 8, the chances of getting breast cancer by age 50 are 1 in 54. By age 60 the chances are 1 in 23. In the 1990's, the breast cancer death rate declined by the largest amount in over 65 years. Heart disease, not breast cancer, is the leading killer of women. Women under the age of 40 account for only 5% of breast cancer cases. Nearly 97% of women who are diagnosed with breast cancer at an early stage survive for more than 5 years.

Signs and Symptoms

[span class=alert]The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.[/span]

The primary sign or symptom associated with breast cancer is finding a breast lump. In a survey of post-mastectomy women, the first sign or symptom of breast cancer was identified by the patient herself 80% of the time. In 19% of cases, the first signs were picked up by health professionals. In 1% of cases, the first clues were identified by lovers. An unexpected finding was that pain was the first symptom noted by 13% of the women. (9)

No symptoms may be present

  • A breast lump may be found upon routine self-examination
  • Pain or tenderness may be present in the breast
  • If a lump is found by self exam or mammogram, a biopsy is necessary to determine if the lump is cancer

Treatment Options


There are four primary types of treatment for breast cancer, which include:

    surgery (lumpectomy, partial mastectomy, radical mastectomy) radiation therapy (using high-dose x-rays to kill cancer cells) chemotherapy (numerous forms of cytotoxic drugs are used to kill cancer cells) hormonal therapy (using anti-estrogen drugs or surgically removing the ovaries)

Estrogen Receptors
The cells of many breast cancers have a chemical “socket" or receptor for estrogen on their surface. The presence of this receptor is usually determined by the pathologist during an examination of the biopsy tissue. Roughly 50 to 70% of breast cancers have estrogen receptors and are referred to as being estrogen receptor positive (ER+). Breast cancer cells that lack estrogen receptors are called estrogen receptor negative (ER-). ER+ breast cancers are stimulated by the presence of estrogen more than ER- breast cancers.

Cutting off the estrogen supply to ER+ breast tumors often stops or substantially slows down their growth rate. This is important because two-thirds of patients with ER+ tumors respond to hormonal therapy, compared to less than 10% with ER-. (10) Therefore, being estrogen receptor positive is provides a substantially better prognostic outcome than ER- status.

Anti-estrogen medications:

Tamoxifen appears to act by binding to estrogen receptor sites on cells. It has been used for over 20 years to treat estrogen receptor positive breast cancer and is probably the most commonly prescribed anticancer medication in the world.

Selective estrogen receptor modulators (SERM 2), such as raloxifene, have been developed for the prevention of osteoporosis. Preliminary studies with raloxifen revealed that the breast cancer rate was also reduced by more than 50% without any increase in endometrial cancer. The search for a SERM 3, and beyond, may lead to the development of drugs that have the beneficial effects of estrogen while preventing breast cancer and osteoporosis. (11)

Additional therapies:

Bone marrow transplant is a procedure that is sometimes attempted when a woman becomes resistant to chemotherapy. This procedure involves taking a sample of a patient’s bone marrow and freezing. After the patient has undergone extremely high doses of chemotherapy, which destroys the bone marrow, the bone marrow cells are injected back into the patient, in the hopes that they will stimulate the production of healthy new cells.

Peripheral blood stem cell transplant. The patient's blood is passed through a machine that removes the stem cells (immature cells from which all blood cells develop) and then returns the blood back to the patient. This procedure is called leukapheresis and usually takes 3 or 4 hours to complete. The stem cells are treated with drugs to kill any cancer cells and then frozen until they are transplanted back to the patient. This procedure may be done alone or with a bone marrow transplant.

Early Detection: Women are encouraged to adhere to the following guidelines regarding the early detection of breast cancer. These include (a) annual physical breast exam by a physician,(b) annual mammography for women over 40 years of age according to the prescribed guidelines, and (c) monthly breast self-examination (BSE). When a woman does all three of these things, she's doing everything she can to insure early detection of breast cancer.

Risk factors:

The risk factors for breast cancer can be divided into two categories, uncontrollable and controllable. The major uncontrollable risk factors are related to issues involving gender and a woman’s menstrual, reproductive, and family history.
GENDER: Most breast cancers (over 99%) occur in women. Recent statistics from the American Cancer Association indicate that approximately 1,400 men are diagnosed with breast cancer annually and 400 men die from breast cancer. (12)
AGE: The longer a woman lives, the more likely she is to develop breast cancer.
FAMILY HISTORY: A gene defect is suspected when two or more first-degree relatives have developed premenopausal breast cancer. The term first-degree refers to parents, siblings, or children. If a woman has a first-degree relative with premenopausal breast cancer, her risk is 6 to 7 times greater than those with no such family history. Postmenopausal breast cancer is not thought to be due to defective genes. Having a single blood relative with breast cancer has very little relative risk, perhaps only 1.5 times greater.
DEFECTIVE GENES: It is estimated that breast cancer caused by gene defects is estimated to account for only 5 to 10% of all breast cancer cases. If a woman has inherited a mutated gene from either parent, she is more likely to develop breast cancer. According to the American Cancer Society, about 50%-60% of women with these inherited gene mutations will develop breast cancer by the age of 70.
EARLY ONSET OF MENSTRUATION: Women who begin menstruating before the age of twelve have a much greater risk of developing breast cancer compared to a woman who began menstruating at age 13 or older. (13)
LATE MENOPAUSE: Women who experience menopause after the age of fifty have double the breast cancer risk of women with earlier menopause. (14)
LATE CHILDBEARING: A woman who gives birth to her fist child after age 30 has a four times greater risk of breast cancer than one who has her first child before the age of 18. Women who never bear children have an even greater risk. (15)

The controllable risk factors for breast cancer, such as diet, nutrition, exercise, alcohol consumption, etc. are discussed in the lifestyle section of this monograph.

Nutritional Suplementation

Antioxidant Nutrients

Antioxidant nutrients help support the immune system, especially when the body is under stress. Although the following research highlights individual antioxidant nutrients, it should be stressed that it is not advisable to take large amounts of one or two antioxidants while excluding the rest. For optimal protection, a nutritional supplement program should include multiple antioxidants. The primary antioxidants are vitamins A, C, E, beta-carotene, selenium, coenzyme Q10, and lipoic acid.

In the following 18-month study, 32 women with breast cancer were put on a nutritional protocol consisting of high dose antioxidants and accessory nutrients. The women were between 32 and 81 years of age and classified “high risk" because of tumor spread to the lymph nodes in the axilla. The nutritional protocol, which was added to the normal surgical and therapeutic treatments for breast cancer, consisted of a combination of the following antioxidants. Vitamin C, 2,850 mg; vitamin E, 2500 IU; beta-carotene, 32.5 IU selenium, 387mcg, plus secondary vitamins and minerals, essential fatty acids (1.2 gm gamma linolenic acid and 3.5 gm omega-3 fatty acids) and coenzyme Q10, (90mg per day). Biochemical markers, clinical condition, tumor spread, quality of life parameters, and survival were followed during the 18-month trial. Compliance was excellent. The main observations were: none of the patients died during the study period (the expected number was four); none of the patients showed signs of further distant metastases; quality of life was improved (no weight loss, reduced use of painkillers); and six patients showed apparent partial remission. (16)

Vitamin E

Vitamin E, although best known as an antioxidant, has been reported to have several functions that are unrelated to its antioxidant activity. Recent studies indicate that vitamin E may inhibit smooth muscle cell and also cancer cell growth. In both breast and prostate cell cancer lines, analysis revealed extensive fragmentation, indicating death of all cell lines supplemented with vitamin E. These studies give evidence of a general inhibition of cell growth by dl-alpha-tocopherol, with breast and prostate cancer cells. (17)


It has been suggested that selenium levels in the blood might be used as a non-invasive diagnostic parameter in clinical assessment of malignant breast disease. The results of one study revealed that women with breast cancer had blood selenium levels ranging from 41-58mcg/l, whereas the selenium levels in healthy women subjects ranged from 73-89mcg/l. (18) However, other studies suggest that selenium intake later in life is not likely to be an important factor in the etiology of breast cancer.

Coenzyme Q10 (CO-Q10)

Coenzyme Q10 (CoQ10) was part of the therapy in the previously mentioned nutritional/antioxidant protocol with women who were “high-risk" breast cancer patients. Six of the 32 women in that trial reported partial tumor regression. In one of those six women, the dosage of CoQ10 was increased to 390mg. In one month, her tumor was no longer palpable and in another month, mammography confirmed the absence of tumor. (19)


Melatonin is a hormone that is secreted from the pineal gland in the brain. Melatonin is the “sleep trigger"- the substance that regulates the sleep/wake cycle. However, recent research also indicates that melatonin is also an antioxidant. (20) Studies report that melatonin is capable of inhibiting the in vitro growth of breast cancer cells, suggesting that it may be useful in the prevention of breast cancer. (21)

Soy Isoflavones

In cultures where soy products are consumed in abundance, women’s health problems, certain cancers, and cardiovascular disease are reported to be less prevalent. (22) Consuming more soy products in the diet increases the amount of phytoestrogens that you get, which act similar to the natural estrogens found in the body only weaker. Soy isoflavones, such as genistein and daidzein are rich in phytoestrogens and are thought to reduce the symptoms of menopause, support healthy bone structure and decrease the risk of certain cancers. (23) , (24) , (25) , (26)

Large studies of particular groups of people have noted that diets with a lot of soy is associated with a lowered risk of cancers, including breast cancer. (27) Evidence in support for these claims has come from animal studies and laboratory studies of breast cancer cells from humans. (28) , (29) , (30) Researchers concluded that in order to reduce the risk of breast cancer, the beneficial effects occur from soy and soy isoflavones in the diet prior to and during puberty. (31)

The soy isoflavone genistein has been shown to stimulate the growth of a particular type of breast cancer in women that is dependent on estrogen. (32) , (33) Genistein has also been shown to cancel out the beneficial effects of tamoxifen in women with certain estrogen positive breast tumors. (34) Therefore, women with estrogen positive breast cancer or who are on tamoxifen should discuss the use of isoflavones with their healthcare professional.


Flaxseed is a good source of plant lignans, particularly secoisolariciresinol and matairesinol, which are then converted to the lignans enterodiol, enterolactone once inside the body. (35) They are similar in structure to sex hormones and thus behave similar to estrogen or possibly block the effects of estrogen. This activity alters the breakdown of hormones and thus possibly decreases any related cancer risk. (36) , (37) , (38)

One study suggested that the reduced risk may result from changing the breakdown of estrogen to 2-hydroxyestrogen and 16alpha-hydroxyestrone. 2-hydroxyestrogen may also have breast cancer protective effects due to its slight estrogen effect and possible anti-estrogen activity. (39) A study involving more than 280 women noted a substantial reduction in breast-cancer risk among women with a diet high in the lignan enterolactone. (40) Since increased concentrations of insulin-like growth factor I (IGF-I) are associated with an increased risk of breast cancer, another possible way in which flaxseed decreases the risk of breast cancer is by reducing the amount of IGF-I in the blood. (41) Other studies, mainly using animals have demonstrated inhibited growth and delayed progression of breast tumors. (42) , (43)

Herbal Suplementation


Arabinoxylane is a dietary fiber from the outer shell of rice bran that has been modified with from three different medicinal mushrooms including; Shiitake, Kawaratake and Suehirotake. The altered arabinoxylane is studied and marketed as MGN-3 and has the potential to support immune system in cancer patients receiving chemotherapy. (44) Arabinoxylane has been reported to improve Natural Killer (NK) cell activity, increase production of tumor necrosis factor-a (TNF-a) and increase interferon-g (IFN-g) synthesis. (45) , (46) , (47)

Shiitake Mushroom

Shiitake mushroom grows on the trunks or stumps of trees, with the medicinal part used being the mycelia or immature growing stage of the mushroom. Shiitake has been used in Traditional Chinese Medicine for thousands of years as a medicinal agent. Shiitake mycelia has been reported to be immunomodulating in the following ways: 1. Activation of macrophages, promoting recognition of antigens, and information transmission to the T-helper cells, increasing rate of phagocytosis, 2. Increase and reinforce interleukin-1 production, thereby activating the T-helper cells, 3. Promotes the mitosis and proliferation of B-lymphocytes, 4. Increases antibody production. (48) , (49)

Larch Arabinogalactan

Arabinogalactans are a class of long, densely branched polysaccharides. Because of the immune-enhancing properties, larch arabinogalactan (LA) is receiving increased attention as a potentially useful immune system enhancer and addition to more traditional cancer treatment options. LA is reported to enhance immunity by various methods, including stimulating the activity of natural killer cells and inhibiting the spread of tumor cells to the liver. (50)

Green Tea

Green tea reportedly has antioxidant properties (51) and the ability to protect against oxidative damage of red blood cells. (52) Antioxidants protect cells and tissues against oxidative damage and injury. (53) Green tea’s antioxidant effects seem to be dependent upon the polyphenol (catechin) fraction. (54) , (55) It is important to note that the addition of milk to any tea may significantly lower the antioxidant potential. (56)

Investigators have reported that increased consumption of green tea was associated with decreased numbers of axillary lymph node metastases among pre-menopausal women with stage I and II breast cancer and with increased expression of progesterone and estrogen receptors among postmenopausal women. (57) , (58) Claims have been made that increased consumption of green tea prior to clinical cancer onset may be associated with improved prognosis of stage I and II breast cancer. This association may be related to a modifying effect of green tea on the clinical characteristics of the cancer. (59)

Diet & Lifestyle

The following lifestyle factors are important for women who want to reduce their risk of developing breast cancer. However, this information is also very important for women who have already been diagnosed with breast cancer, because the factors discussed below can alter hormone activity, boost the immune system, and increase women’s chances for successful remission and long-term survival.

Dietary factors affect a woman’s risk of breast cancer. These include the following:

Dietary Fat: Most epidemiological studies on breast cancer have reported that high fat-consuming societies have higher rates of cancer. Research indicates that dietary fat tends to promote tumorigenesis, but only certain types of tumors, such as mammary tumors. (60) Societies with low cancer rates consume 20 percent or less of their daily calories from fat.

However, consideration for the significance of “good" fats and “bad" fats should be noted. Experimental evidence from animal and human trials indicate that excess omega-6 fats and oils increase the risk of cancers of the breast, prostate, and colon, whereas omega-3 fats and oils seem to be cancer-protective. Studies also indicate that high consumption of omega-6 polyunsaturated fatty acids (PUFAs) stimulates several stages in the development of mammary and colon cancer, from an increase in oxidative DNA damage to effects on cell proliferation, free estrogen levels to hormonal catabolism. In contrast, fish oil-derived omega-3 fatty acids seem to prevent cancer by influencing the activity of enzymes and proteins related to intracellular signaling, and ultimately, cell proliferation. (61) Rather than trying to eliminate fats, the emphasis should be on ingesting optimal amounts of the right kind of fats. In general, most people in the U.S. consume too much of the omega-6 fats (corn, safflower, sunflower oils) and not enough of the omega-3 fats. The best sources for omega-3 fats are flaxseed oil (one tablespoonful daily) and fish oil capsules containing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).

Fiber: The conclusion of many researchers is that fiber fights cancer. A high fiber diet acts to decrease the amount of estrogen in a woman’s body. Estrogens circulating in the blood pass through the liver, where they are bound into biologically inactive compounds. These inactive estrogen complexes are then passed via the bile into the intestines for excretion. However, intestinal bacteria can free up much of this estrogen, making it available for reabsorption. (62) Research suggests that the amount of fiber in the diet affects the activity of intestinal bacteria, which in turn affects the amount of estrogen that gets reabsorbed. The intestinal bacteria that proliferate in meat-eating women are more capable of freeing up the previously bound estrogen, which increases estrogen levels and a woman’s risk of breast cancer. (63)

Sugar has been implicated as a dietary link to breast cancer. The results of a study that evaluated food consumption statistics from 21 countries found a strong association between sugar consumption and breast cancer in postmenopausal women. The fact that women with adult onset diabetes have a higher incidence of breast cancer supports the sugar/breast cancer hypothesis. (64)

Toxins in food and water as well as environmental exposures represent an increased risk of breast cancer. Some of the worst offenders are the chemicals that belong to a class of compounds known as organochlorines. These are fat-soluble compounds that that get stored in fatty tissue, and a woman’s breast tissue is a prime storage site for these toxins. Research revealed that women with higher blood levels of DDE, which is a metabolite of DDT, have up to a four times greater risk of developing breast cancer. (65) Research funded by the World Health Organization and published in 1976 revealed that DDT and other pesticides were found in very high concentrations in the tumors of women with breast cancer. (66) This does not allow the conclusion that all breast cancer is due to pesticide toxicity to be drawn.

In a paper entitled, “Organochlorine Contamination of Breast Milk," the authors state that over 95 percent of all the toxic chemicals ingested in the American diet come from meat, fish, eggs, and dairy products. (67)

Exercise: Regular exercise lowers circulating levels of estrogen and reduces a woman’s risk of developing breast cancer. A study published in the September 21, 1994 issue of the Journal of the National Cancer Institute reported that moderate regular exercise resulted in a substantial reduction of a premenopausal woman’s risk of developing breast cancer. (68) In another study, Dr. Rose Frisch at the Harvard School of Public Health examined the occurrence of breast cancer among female college athletes compared to non-athletes. The data was gathered from 5,398 women (2,622 former college athletes and 2,776 non-athletes) who were alumnae from eight different colleges from 1925 to 1981. The women non-athletes had an 86 percent greater occurrence of breast cancer than the women who had been athletes. (69)

It is important to emphasize to women that even moderate levels of regular exercise can provide substantial reduction in the future risk of breast cancer. This is especially true for adolescent girls. When regular exercise programs are started in adolescence, moderate levels of regular physical activity can produce beneficial changes in menstrual cycle patterns and female hormones, which significantly lowers the risk of breast cancer later in life. (70) , (71)

Alcohol consumption can increase circulating estrogen levels and increase a woman’s risk of developing breast cancer. The results of one study revealed that regular consumption of 30 grams of alcohol per day, which is equivalent to approximately two average drinks, increased levels of estrogen excreted in the urine. (72) In the Nurses Health Study, researchers followed 89,538 women between the ages of 34 and 59 for a number of years. The results revealed that women who consumed between three and nine drinks per week were 30 percent more likely to develop breast cancer. (73)

In a comprehensive review of the scientific literature, Dr.Lynn Rosenberg stated that the association between alcohol and breast cancer is real, although rather weak. (74) Another literature review reported that five out of six epidemiological studies have found a positive correlation between alcohol consumption and increased risk for breast cancer. In the same review in which 28 case-controlled studies were examined, 18 of the studies reported a positive association between alcohol consumption and breast cancer, whereas 10 studies did not. (75)


  1. View Abstract: Feig SA. DUCTAL CARCINOMA IN SITU Implications for Screening Mammography. Radiol Clin North Am. Jul2000;38(4):653-68.
  2. View Abstract: McKenna RJ, Sr. The abnormal mammogram radiographic finding, diagnostic options, pathology, and stage of cancer diagnosis. Cancer. 1994;74:244-255.
  3. View Abstract: Holt JT, et al. Histopathology: Old principles and new methods. Cancer Surveys. 1993;18:115-133.
  4. Abeloff MD, Lichter JS, Niederhuber JE, Pierce LJ, Love RR. Breast. In: Abeloff MD, Armitage JO, Lichter JS, et al, eds. Clinical Oncology. 2nd ed. New York: Churchill Livingston; 2000:2088.
  5. American Cancer Society. The Staging of Cancer. Publication 89-12M, No. 3485.01.
  6. American Cancer Society: Cancer Facts and Figures 2006;
  7. American Cancer Society: Cancer Facts and Figures 2006;
  8. American Cancer Society: Cancer Facts and Figures 2006;
  9. View Abstract: Bullough B. Discovery of the first signs and symptoms of breast cancer. Nurse Pract. Nov1980;5(6):31-2,47.
  10. View Abstract: Morgan LR, Jr, et al. Therapeutic use of tamoxifen in advanced breast cancer: Correlation with biochemical parameters. Cancer Treatment Report. 1976;60:1437.
  11. View Abstract: Osborne MP. Breast cancer prevention by antiestrogens. Ann N Y Acad Sci. 1999;889:146-51.
  12. American Cancer Society. Cancer Facts & Figures. 2000.
  13. View Abstract: Pike MC, et al. Oral contraceptive use and early abortion as risk factors for breast cancer in young women. British Journal of Cancer. 1981;43:72-76.
  14. Kelsey JL, Hildredth NG. Breast and Gynecologic Cancer Epidemiology. Boca Raton, Fl: CRC Press; 1983:138-140.
  15. MacMahon B, et al. Age at first birth and breast cancer risk. World Health Organization Bulletin. 1970;43:209-221.
  16. View Abstract: Lockwood K, et al. Apparent partial remission of breast cancer in 'high risk' patients supplemented with nutritional antioxidants, essential fatty acids and coenzyme Q10. Mol Aspects Med. 1994;15 Suppl:s231-40.
  17. View Abstract: Sigounas G, et al. dl-alpha-tocopherol induces apoptosis in erythroleukemia, prostate, and breast cancer cells. Nutr Cancer. 1997;28(1):30-5.
  18. Krsnjavi H, Becker D. Serum selenium level as a diagnostic parameter in breast cancer. Helv Chir Acta. May1992;59(1):231-4.
  19. View Abstract: Lockwood K, et al. Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q10. Biochem Biophys Res Commun. Mar1994;199(3):1504-8.
  20. View Abstract: Antunes F, et al. On the antioxidant activity of melatonin. Free Radic Biol Med. Jan1999;26(1-2):117-28.
  21. View Abstract: Cos S, et al. Melatonin, experimental basis for a possible application in breast cancer prevention and treatment. Histol Histopathol. Apr2000;15(2):637-47.
  22. View Abstract: Barnes S. Evolution of the health benefits of soy isoflavones. Proc Soc Exp Biol Med. 1998;217:386-398.
  23. View Abstract: Kritz-Silverstein D, Goodman-Gruen DL. Usual dietary isoflavone intake, bone mineral density, and bone metabolism in postmenopausal women. J Womens Health Gend Based Med. Jan2002;11(1):69-78.
  24. View Abstract: Adlercreutz H. Phytoestrogens: Epidemiology and a possible role in cancer protection. Environ Health Perspect. 1995;103S:103-112.
  25. View Abstract: Cotroneo MS, Wang J, Fritz WA, Eltoum IE, Lamartiniere CA. Genistein action in the prepubertal mammary gland in a chemoprevention model. Carcinogenesis. Sep2002;23(9):1467-1474.
  26. View Abstract: Wu AH, Wan P, Hankin J, Tseng CC, Yu MC, Pike MC. Adolescent and adult soy intake and risk of breast cancer in Asian-Americans. Carcinogenesis. Sep2002;23(9):1491-6.
  27. View Abstract: Messina MJ, Persky V, Setchell KDR. Soy Intake and Cancer Risk: A Review of the in Vitro and in Vivo Data. Nutr Cancer. 1994;21:113.
  28. View Abstract: Peterson TG, et al. Metabolism of the isoflavones genistein and biochanin A in human breast cancer cell lines. Am J Clin Nutr. 1998;68(6 Suppl):1505S-1511S.
  29. View Abstract: Barnes S. Effect of genistein on in vitro and in vivo models of cancer. J Nutr. 1995;125(3 Suppl):777S-783S.
  30. View Abstract: Barnes S. The chemopreventive properties of soy isoflavonoids in animal models of breast cancer. Breast Cancer Res Treat. 1997;46:169-170.
  31. View Abstract: Brown NM, et al. Xenoestrogens alter mammary gland differentiation and cell proliferation in the rat. Environ Health Perspect. 1995;103:708-713.
  32. View Abstract: Allred CD, Allred KF, Ju YH, et al. Soy diets containing varying amounts of genistein stimulate growth of estrogen-dependent (MCF-7) tumors in a dose-dependent manner. Cancer Res. Jul2001;61(13):5045-50.
  33. View Abstract: Hsieh CY, Santell RC, Haslam SZ, Helferich WG. Estrogenic effects of genistein on the growth of estrogen receptor-positive human breast cancer (MCF-7) cells in vitro and in vivo. Cancer Res. Sep1998;58(17):3833-8.
  34. View Abstract: Ju YH, Doerge DR, Allred KF, Allred CD, Helferich WG. Dietary Genistein Negates the Inhibitory Effect of Tamoxifen on Growth of Estrogen-dependent Human Breast Cancer (MCF-7) Cells Implanted in Athymic Mice. Cancer Res. May2002;62(9):2474-7.
  35. View Abstract: Hutchins AM, Martini MC, Olson BA, Thomas W, Slavin JL. Flaxseed influences urinary lignan excretion in a dose-dependent manner in postmenopausal women. Cancer Epidemiol Biomarkers Prev. Oct 2000;9(10):1113-8.
  36. View Abstract: Hutchins AM, Martini MC, Olson BA, Thomas W, Slavin JL. Flaxseed consumption influences endogenous hormone concentrations in postmenopausal women. Nutr Cancer. 2001;39(1):58-65.
  37. View Abstract: Lampe JW, Martini MC, Kurzer MS, Adlercreutz H, Slavin JL. Urinary lignan and isoflavonoid excretion in premenopausal women consuming flaxseed powder. Am J Clin Nutr. Jul 1994;60(1):122-8.
  38. View Abstract: Haggans CJ, Hutchins AM, Olson BA, Thomas W, Martini MC, Slavin JL. Effect of flaxseed consumption on urinary estrogen metabolites in postmenopausal women. Nutr Cancer. 1999;33(2):188-95.
  39. View Abstract: Haggans CJ, Travelli EJ, Thomas W, Martini MC, Slavin JL. The effect of flaxseed and wheat bran consumption on urinary estrogen metabolites in premenopausal women. Cancer Epidemiol Biomarkers Prev. Jul 2000;9(7):719-25.
  40. View Abstract: Ingram D, Sanders K, Kolybaba M, Lopez D. Case-control study of phyto-oestrogens and breast cancer. Lancet. 4 Oct 1997;350(9083):990-4.
  41. View Abstract: Rickard SE, Yuan YV, Thompson LU. Plasma insulin-like growth factor I levels in rats are reduced by dietary supplementation of flaxseed or its lignan secoisolariciresinol diglycoside. Cancer Lett. Dec 2000;161(1):47-55.
  42. View Abstract: Mousavi Y, Adlercreutz H. Enterolactone and estradiol inhibit each other's proliferative effect on MCF-7 breast cancer cells in culture. J Steroid Biochem Mol Biol. Mar 1992;41(3-8):615-9.
  43. View Abstract: Rickard SE, Yuan YV, Chen J, Thompson LU. Dose effects of flaxseed and its lignan on N-methyl-N-nitrosourea-induced mammary tumorigenesis in rats. Nutr Cancer. 1999;35(1):50-7.
  46. Ghoneum M, et al. NK IMMUNOMODULATORY FUNCTION IN 27 CANCER PATIENTS BY MGN-3, A MODIFIED ARABINOXYLANE FROM RICE BRAN, 87th Annual Meeting of the American Association for Cancer Research. Washington,DC. Apr1996.
  48. Suzuki H, et al. Immunopotentiating Substances in Lentinus edodes Mycelial Extract (LEM)-- Activation of Macrophage and Proliferation of Bone Marrow Cell. Nippon Shokakibyo Gakkai Zasshi. Jul1988;85(7):1430.
  49. View Abstract: Suzuki H, et al. Inhibition of the Infectivity and Cytopathic Effect of Human Immunodeficiency Virus by Water-soluble Lignin in an Extract of the Culture Medium of Lentinus edodes Mycelia (LEM). Biochem Biophys Res Commun. Apr1989;160(1):367-373.
  50. View Abstract: Hauer J, et al. Mechanism of Stimulation of Human Natural Killer Cytotoxicity by Arabinogalactan from Larix occidentalis. Cancer Immunol Immunother. 1993;36(4):237-44.
  51. Cheng TO. Antioxidants in Chinese Green Tea. J Am Coll Cardiol. Apr1998;31(5):1214.
  52. View Abstract: Grinberg LN, et al. Protective Effects of Tea Polyphenols against Oxidative Damage to Red Blood Cells. Biochem Pharmacol. Nov1997;54(9):973-78.
  53. View Abstract: Halliwell B. How to Characterize an Antioxidant: An Update. Biochem Soc Symp. 1995;61:73-101.
  54. View Abstract: Kumamoto M, et al. Evaluation of the Antioxidative Activity of Tea by an Oxygen Electrode Method. Biosci Biotechnol Biochem. Jan1998;62(1):175-77.
  55. View Abstract: Hirayama O, et al. Evaluation of Antioxidant Activity by Chemiluminescence. Anal Biochem. May1997;247(2):237-41.
  56. View Abstract: Hertog MG, et al. Antioxidant Flavonols and Ischemic Heart Disease in a Welsh Population of Men: The Caerphilly Study. Am J Clin Nutr. May1997;65(5):1489-94.
  57. View Abstract: Nakachi K, et al. Influence of Drinking Green Tea on Breast Cancer Malignancy among Japanese Patients. Jpn J Cancer Res. Mar1998;89(3):254-61.
  58. View Abstract: Nagata C, et al. Association of Coffee, Green Tea, and Caffeine Intakes with Serum Concentrations of Etradiol and Sex Hormone-binding Globulin in Premenopausal Japanese Women. Nutr Cancer. 1998;30(1):21-24.
  59. Mukhtar H, et al. Cancer Chemoprevention by Green Tea Components. Adv Exp Med Biol. 1994;354:123-34.
  60. View Abstract: Ip C. Controversial issues of dietary fat and experimental mammary carcinogenesis. Prev Med. Sep1993;22(5):728-37.
  61. View Abstract: Bartsch H, et al. Dietary polyunsaturated fatty acids and cancers of the breast and colorectum: emerging evidence for their role as risk modifiers. Carcinogenesis. Dec1999;20(12):2209-18.
  62. View Abstract: Goldin BR, et al. Estrogen excretion patterns and plasma levels in vegetarian and omnivorous women. N Engl J Med. Dec1982;307(25):1542-7.
  63. View Abstract: Gorbach SL. Estrogens, breast cancer, and intestinal flora. Rev Infect Dis. Mar1984;6 (Suppl 1):S85-90.
  64. View Abstract: Seely S, Horrobin DF. Diet and breast cancer: the possible connection with sugar consumption. Med Hypotheses. Jul1983;11(3):319-27.
  65. View Abstract: Wolff MS, et al. Blood levels of organochlorine residues and risk of breast cancer. Journal of the National Cancer Institute. 1993;85(8):648-652.
  66. Wassermann M, et al. Organochlorine compounds in neoplastic and adjacent apparently normal breast tissue. Bulletin of Environmental Contamination Toxicology. 1976;15:478-84.
  67. Harris S. Organochlorine Contamination of Breast Milk. Environmental Defense Fund. Washington DC. 1979.
  68. View Abstract: Bernstein L, et al. Physical exercise and reduced risk of breast cancer in young women. Journal of the National Cancer Institute. 1994;86(18):1403-1408.
  69. View Abstract: Frisch RE, et al. Lower prevalence of breast cancer and cancers of the reproductive system among former college athletes compared to non-athletes. British Journal of Cancer. 1985;52:885-891.
  70. View Abstract: Bernstein L, et al. The effects of moderate physical activity on menstrual cycle patterns in adolescence: Implications for breast cancer prevention. British Journal of Cancer. 1987;55:681-685.
  71. View Abstract: Dorn J, et al. Lifetime Physical Activity and Breast Cancer Risk in Pre- and Postmenopausal Women. Medicine & Science in Sports & Exercise. 2003;35(2):278-285.
  72. View Abstract: Reichman ME, et al. Effects of alcohol consumption on plasma and urinary hormone concentrations in premenopausal women. Journal of the National Cancer Institute. 1993;85(9):722-27.
  73. View Abstract: Willett WC, et al. Moderate alcohol consumption and the risk of breast cancer. New England Journal of Medicine. 1987;316:1174-80.
  74. Rosenberg L, et al. Alcohol consumption and risk of breast cancer: A review of the epidemiologic evidence. Epidemiologic Reviews. 1993;15:133-44.
  75. View Abstract: Friedenreich CM, et al. A cohort study of alcohol consumption and risk of breast cancer. American Journal of Epidemiology. 1993;137(5):512-20.