General Information
Patient evaluation
Contralateral disease
Hormone replacement therapy
Genetics
Follow-up
Breast reconstruction
Note: Separate PDQ summaries on Prevention of Breast Cancer; Screening for
Breast Cancer; Breast Cancer and Pregnancy Treatment; and Male Breast Cancer
Treatment are also available.
Note: Estimated new cases and deaths from breast cancer (women only) in the United States in 2004:[1] - New cases: 215,990.
- Deaths: 40,110.
Note: Some citations in the text of this section are followed by a level of
evidence. The PDQ editorial boards use a formal ranking system to help the
reader judge the strength of evidence linked to the reported results of a
therapeutic strategy. (Refer to the PDQ summary on Levels of Evidence for more
information.)
Several well-established factors have been associated with an increased risk of
breast cancer. These include family history, nulliparity, early menarche,
advanced age, and a personal history of breast cancer (in situ or invasive).
(Refer to the PDQ summary on Genetics of Breast and Ovarian Cancer for more
information.)
Clinical trials have established that screening with mammography, with or
without clinical breast examination, may decrease breast cancer mortality.
(Refer to the PDQ summary on Screening for Breast Cancer for more information.)
Breast cancer is commonly treated by various combinations of surgery, radiation
therapy, chemotherapy, and hormone therapy. Prognosis and selection of therapy
may be influenced by the age and menopausal status of the patient, stage of the
disease, histologic and nuclear grade of the primary tumor, estrogen-receptor
(ER) and progesterone-receptor (PR) status, measures of proliferative capacity,
and HER2/neu gene amplification.[2] Although certain rare inherited mutations
such as BRCA1 and BRCA2 predispose women to develop breast cancer, prognostic
data on mutation carriers who have developed breast cancer are conflicting.
Since criteria for menopausal status vary widely, some studies have substituted
age older than 50 years as a surrogate for the postmenopausal state. Breast
cancer is classified into a variety of histologic types, some of which have
prognostic importance. For example, favorable histologic types include
mucinous, medullary, and tubular carcinoma.[3] This section will discuss only
primary epithelial breast cancers. Rarely, the breast may be involved by other
tumors such as lymphoma, sarcoma, or melanoma. These diseases are discussed
elsewhere in PDQ under the specific disease types.
Patient evaluation
Patient management following initial suspicion of breast cancer generally
includes confirmation of the diagnosis, evaluation of stage of disease, and
selection of therapy. Diagnosis may be made by use of established prognostic
markers. At the time the tumor tissue is surgically removed, ER and PR status
should be determined.
Contralateral disease
Pathologically, breast cancer can be a multicentric and bilateral disease.
Bilateral disease is somewhat more common in patients with infiltrating lobular
carcinoma. Therefore, patients who have breast cancer should have bilateral
mammography at the time of diagnosis to rule out synchronous disease. Patients
should continue to have regular breast physical examinations and mammography to
detect either recurrence in the ipsilateral breast in those patients treated
with breast-conserving surgery or a second primary cancer in the contralateral
breast.[4] The risk of a primary breast cancer in the contralateral breast is
approximately 1% per year.[5,6] Patient age younger than 55 years at the time
of diagnosis or lobular tumor histology appear to increase this risk to
1.5%.[7] The development of a contralateral breast cancer is associated with
an increased risk of distant recurrence.[8,9]
Hormone replacement therapy
The use of hormone replacement therapy (HRT) poses a dilemma for the rising
numbers of breast cancer survivors, many of whom enter menopause prematurely as
a result of therapy. HRT has generally not been used for women with a history
of breast cancer because estrogen is a growth factor for most breast cancer
cells in the laboratory; however, empiric data on the safety of HRT after breast cancer are limited.[10,11] The only reported randomized trial comparing HRT to no hormonal supplementation included 345 evaluable breast cancer patients with menopausal symptoms and was terminated early because of an increased incidence of recurrences and new primaries in the HRT group (hazard ratio 3.5; 95% confidence interval (CI) 1.5-7.4).[12] [Level of evidence: 1iiDi] In total, 26 women in the HRT group and 7 in the non-HRT group developed recurrences or new primaries. This study, however, was not double-blinded, and it is possible that patients on HRT were monitored more closely. Further, a companion trial of similar design did not show an increased risk. This second trial has not been reported. Until and if further data become available, decisions concerning the use of HRT in patients with breast cancer will have to be based on the results of this one study and on inferences from the impact of HRT use on breast cancer risk in other settings.[13] A comprehensive intervention,
including education, counseling, and nonhormonal drug therapy, has been shown
to reduce menopausal symptoms and to improve sexual functioning in breast
cancer survivors.[14] [Level of evidence: 1iiC]
Genetics
Women with a family history of breast cancer may have an increased risk of
disease. Age-specific risk estimates are available to help counsel and design
screening strategies for these women.[15,16] It is estimated that
5% to 10% of all women with breast cancer may have a germ-line
mutation of the genes BRCA1 and BRCA2.[17] Specific mutations of BRCA1 and
BRCA2 are more common in women of Jewish ancestry.[18] The estimated lifetime
risk of developing breast cancer for women with BRCA1 and BRCA2 mutations is
40% to 85%. Carriers with a history of breast cancer have an increased risk of
contralateral disease that may be as high as 5% per year.[19] Male carriers of
BRCA2 mutations are also at increased risk for breast cancer.[20] Mutations in
either gene also confer an increased risk of ovarian cancer.[20-22] In
addition, mutation carriers may be at increased risk of other primary
cancers.[20,22] Genetic testing is available to detect mutations in members of
high-risk families.[23-27] Such individuals should first be referred for
counseling.[28] (Refer to the PDQ summaries on Screening for Breast Cancer;
Prevention of Breast Cancer; and Genetics of Breast and Ovarian Cancer for more
information.)
Follow-up
There is evidence from randomized trials that periodic follow-up with bone
scans, liver sonography, chest x-rays, and blood tests of liver function do not
improve survival or quality of life when compared to routine physical
examinations.[29,30] Even when these tests permit earlier detection of
recurrent disease, patient survival is unaffected.[30] Based on these data,
some investigators recommend that acceptable follow-up be limited to physical
examination and annual mammography for asymptomatic patients who complete
treatment for stages I-III breast cancer. The frequency of follow-up and the
appropriateness of screening tests after the completion of primary treatment
for stages I-III breast cancer remain controversial.
Breast reconstruction
For patients who opt for a total mastectomy, reconstructive surgery may be
used. It may be done at the time of the mastectomy (immediate reconstruction)
or at some subsequent time (delayed reconstruction).[31-34] Breast contour can
be restored by the submuscular insertion of an artificial implant
(saline-filled) or a rectus muscle or other flap. If a saline implant is used,
a tissue expander can be inserted beneath the pectoral muscle. Saline is
injected into the expander to stretch the tissues over a period of weeks or
months until the desired volume is obtained. The tissue expander is then
replaced by a permanent implant. While there is no convincing evidence that a
silicone implant induces cancer or autoimmune disease, silicone implants are
available only through restricted clinical trials approved by the Food and Drug
Administration (visit the FDA’s fda.gov Web site for more
information on silicone breast implants). Rectus muscle flaps require a
considerably more complicated and prolonged operative procedure, and blood
transfusions may be required. Following breast reconstruction, radiation
therapy can be delivered to the chest wall and regional nodes either in the
adjuvant setting or if local disease recurs. Radiation therapy following
reconstruction with a breast prosthesis may affect cosmesis, and the incidence
of capsular fibrosis, pain, or the need for implant removal may be
increased.[35]
References
- American Cancer Society.: Cancer Facts and Figures 2004. Atlanta, Ga: American Cancer Society, 2004. Also available online. Last accessed May 13, 2004.
- Simpson JF, Gray R, Dressler LG, et al.: Prognostic value of histologic grade and proliferative activity in axillary node-positive breast cancer: results from the Eastern Cooperative Oncology Group Companion Study, EST 4189. J Clin Oncol 18 (10): 2059-69, 2000.
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- Rosen PP, Groshen S, Kinne DW: Prognosis in T2N0M0 stage I breast carcinoma: a 20-year follow-up study. J Clin Oncol 9 (9): 1650-61, 1991.
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- Orel SG, Troupin RH, Patterson EA, et al.: Breast cancer recurrence after lumpectomy and irradiation: role of mammography in detection. Radiology 183 (1): 201-6, 1992.
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- Rosen PP, Groshen S, Kinne DW, et al.: Factors influencing prognosis in node-negative breast carcinoma: analysis of 767 T1N0M0/T2N0M0 patients with long-term follow-up. J Clin Oncol 11 (11): 2090-100, 1993.
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- Gustafsson A, Tartter PI, Brower ST, et al.: Prognosis of patients with bilateral carcinoma of the breast. J Am Coll Surg 178 (2): 111-6, 1994.
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- Broët P, de la Rochefordière A, Scholl SM, et al.: Contralateral breast cancer: annual incidence and risk parameters. J Clin Oncol 13 (7): 1578-83, 1995.
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- Healey EA, Cook EF, Orav EJ, et al.: Contralateral breast cancer: clinical characteristics and impact on prognosis. J Clin Oncol 11 (8): 1545-52, 1993.
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- Heron DE, Komarnicky LT, Hyslop T, et al.: Bilateral breast carcinoma: risk factors and outcomes for patients with synchronous and metachronous disease. Cancer 88 (12): 2739-50, 2000.
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- Cobleigh MA, Berris RF, Bush T, et al.: Estrogen replacement therapy in breast cancer survivors. A time for change. Breast Cancer Committees of the Eastern Cooperative Oncology Group. JAMA 272 (7): 540-5, 1994.
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- Roy JA, Sawka CA, Pritchard KI: Hormone replacement therapy in women with breast cancer. Do the risks outweigh the benefits? J Clin Oncol 14 (3): 997-1006, 1996.
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- Holmberg L, Anderson H; HABITS steering and data monitoring committees.: HABITS (hormonal replacement therapy after breast cancer--is it safe?), a randomised comparison: trial stopped. Lancet 363 (9407): 453-5, 2004.
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- Chlebowski RT, Col N: Menopausal hormone therapy after breast cancer. Lancet 363 (9407): 410-1, 2004.
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- Ganz PA, Greendale GA, Petersen L, et al.: Managing menopausal symptoms in breast cancer survivors: results of a randomized controlled trial. J Natl Cancer Inst 92 (13): 1054-64, 2000.
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- Claus EB, Risch N, Thompson WD: Autosomal dominant inheritance of early-onset breast cancer. Implications for risk prediction. Cancer 73 (3): 643-51, 1994.
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- Gail MH, Brinton LA, Byar DP, et al.: Projecting individualized probabilities of developing breast cancer for white females who are being examined annually. J Natl Cancer Inst 81 (24): 1879-86, 1989.
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- Blackwood MA, Weber BL: BRCA1 and BRCA2: from molecular genetics to clinical medicine. J Clin Oncol 16 (5): 1969-77, 1998.
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- Offit K, Gilewski T, McGuire P, et al.: Germline BRCA1 185delAG mutations in Jewish women with breast cancer. Lancet 347 (9016): 1643-5, 1996.
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- Frank TS, Manley SA, Olopade OI, et al.: Sequence analysis of BRCA1 and BRCA2: correlation of mutations with family history and ovarian cancer risk. J Clin Oncol 16 (7): 2417-25, 1998.
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- Cancer risks in BRCA2 mutation carriers.The Breast Cancer Linkage Consortium. J Natl Cancer Inst 91 (15): 1310-6, 1999.
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- Miki Y, Swensen J, Shattuck-Eidens D, et al.: A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1. Science 266 (5182): 66-71, 1994.
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- Ford D, Easton DF, Bishop DT, et al.: Risks of cancer in BRCA1-mutation carriers. Breast Cancer Linkage Consortium. Lancet 343 (8899): 692-5, 1994.
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- Biesecker BB, Boehnke M, Calzone K, et al.: Genetic counseling for families with inherited susceptibility to breast and ovarian cancer. JAMA 269 (15): 1970-4, 1993.
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- Hall JM, Lee MK, Newman B, et al.: Linkage of early-onset familial breast cancer to chromosome 17q21. Science 250 (4988): 1684-9, 1990.
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- Easton DF, Bishop DT, Ford D, et al.: Genetic linkage analysis in familial breast and ovarian cancer: results from 214 families. The Breast Cancer Linkage Consortium. Am J Hum Genet 52 (4): 678-701, 1993.
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- Berry DA, Parmigiani G, Sanchez J, et al.: Probability of carrying a mutation of breast-ovarian cancer gene BRCA1 based on family history. J Natl Cancer Inst 89 (3): 227-38, 1997.
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- Hoskins KF, Stopfer JE, Calzone KA, et al.: Assessment and counseling for women with a family history of breast cancer. A guide for clinicians. JAMA 273 (7): 577-85, 1995.
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- Statement of the American Society of Clinical Oncology: genetic testing for cancer susceptibility, Adopted on February 20, 1996. J Clin Oncol 14 (5): 1730-6; discussion 1737-40, 1996.
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- Impact of follow-up testing on survival and health-related quality of life in breast cancer patients. A multicenter randomized controlled trial. The GIVIO Investigators. JAMA 271 (20): 1587-92, 1994.
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- Rosselli Del Turco M, Palli D, Cariddi A, et al.: Intensive diagnostic follow-up after treatment of primary breast cancer. A randomized trial. National Research Council Project on Breast Cancer follow-up. JAMA 271 (20): 1593-7, 1994.
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- Feller WF, Holt R, Spear S, et al.: Modified radical mastectomy with immediate breast reconstruction. Am Surg 52 (3): 129-33, 1986.
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- Cunningham BL: Breast reconstruction following mastectomy. In: Najarian JS, Delaney JP, eds.: Advances in Breast and Endocrine Surgery. Chicago, Ill: Year Book Medical Publishers, 1986, pp 213-226.
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