eMedicine Specialties > Plastic Surgery > Breast

Breast Cancer

Author: Mary Jo Wright, MD, Associate Professor of Surgery, Chief of Breast Surgery Service, Tulane University School of Medicine; Medical Director, Breast Cancer Center, Medical Center of Louisiana, New Orleans
Coauthor(s): Krzysztof Moroz, MD, Professor of Pathology, Director of Cytopathology, Tulane University Health Sciences Center; R Edward Newsome, MD, Program Director and Chief of Plastic Surgery, Henderson Chair in Surgery, Assistant Dean for Graduate Medical Education, Tulane University School of Medicine
Contributor Information and Disclosures

Updated: Sep 10, 2009

Introduction

History of the Procedure

Over the greater part of the last century, all forms of breast cancer have been treated by aggressive surgical resection. In 1894, Halsted described the procedure of en bloc removal of all breast tissue, draining lymph nodes and pectoralis muscles for the treatment of breast cancer. This technique of radical mastectomy became the standard of care for decades based on an understanding that cancer growth proceeded in stepwise fashion via the lymphatics, thus could be controlled with surgical excision.

In 1971, Fisher et al challenged this standard and demonstrated in the National Surgical Adjuvant Breast and Bowel Project (NSABP) B-04 trial that radical mastectomy had no survival benefit over mastectomy with radiation or mastectomy with delayed axillary dissection.1 In a subsequent study, NSABP B-06, patients were randomized to total mastectomy versus lumpectomy and radiation therapy (XRT), and no survival benefit of total mastectomy was found. However, benefit was observed in the decreased rate of local recurrence in women receiving XRT. Development of new chemotherapeutic and hormonal agents has further revolutionized the management of breast cancer.

For excellent patient education resources, visit eMedicine's Cancer and Tumors Center, Women's Health Center, and Imaging Center. Also, see eMedicine's patient education articles Breast Cancer, Mastectomy, Breast Lumps and Pain, Breast Self-Exam, and Mammogram.

Problem

Worldwide, the overall incidence of breast cancer varies markedly but appears to be rising.2  Far eastern countries such as Japan, which historically have enjoyed low rates in comparison to the United States, are seeing a rapid rise in incidence. Although the United States has the highest reported incidence of breast cancer in the world, several western European nations such as Iceland, Italy, France, Sweden, and the United Kingdom trail closely behind. Incidence has been historically lower in Eastern Europe, the Middle East, and the Far East, but countries such as Japan and Singapore have seen a 2-fold rise over the past few decades.

Frequency

Of American women, 13% will be diagnosed with breast cancer in their lifetimes, making it the most common nonskin cancer among women. In addition, more than 3% will die from the disease. Breast cancer has surpassed lung cancer as the leading cause of cancer death in women worldwide, accounting for more than 400,000 deaths per year. In the United States, breast cancer trails only lung cancer as the second most common cause of cancer death in women. In 2007, more than 1.3 million new cases were diagnosed worldwide. More than 200,000 of these were in the United States alone.

The 1980s saw the greatest rise in incidence, which may have been due to a combination of improvements in screening techniques, data collection, and treatment modalities.3 Despite this surge in newly-diagnosed cases, mortality rates have been declining over the last decade. The decline is widely attributed to earlier detection via screening mammography and improvements in hormonal therapy and cytotoxic chemotherapy.

Etiology

Risk factors for the development of invasive breast cancer include female gender, age, family history, age at the time of first parturition, personal history of previous breast cancer, hormone replacement therapy, history of atypical hyperplasia or noninvasive lesions, and genetics.2,3  

  • Female gender: The incidence of breast cancer in women exceeds that in men by 100:1. Overall, 1 of every 8 American women develops breast cancer in her lifetime.
  • Age: In American women, risk increases from 1:5900 to 1:290 between the third and eighth decades. A woman aged 60-79 years has a 1:14 chance of developing invasive breast cancer, compared with a woman younger than 39 years, who has a 1:225 probability.
  • Age at birth of first child: If aged 30 years or older, relative risk is 2 times that of patients who gave birth when younger than 20 years.
  • Personal history of breast cancer: This also is a recognized risk factor. This factor depends on patient age at time of diagnosis. Risk is increased for younger women.
  • Noninvasive carcinoma (ductal carcinoma in situ [DCIS]/lobular carcinoma in situ [LCIS]) on previous biopsy: This also is a marker for development of invasive lesions.
  • Benign proliferative changes with atypical hyperplasia: These may increase relative risk by 4 times. Atypical hyperplasia may be observed in as many as 10% of specimens from biopsy.
  • Early menarche and late menopause: These also are associated weakly with increased relative risk of breast cancer.
  • Menopausal hormone replacement therapy: Multiple studies, including the Women's Health Initiative and the Million Women Study in the United Kingdom, have shown an increased risk of breast cancer in postmenopausal women who are either recent or current users of estrogen alone or in combination with progestin.4  In addition, the combination use of estrogen with progestin has been associated with an even greater risk of breast cancer, particularly of lobular carcinoma. Increased risk is also related to increased duration of use; this risk can be reduced over time, following the termination of hormone replacement therapy.
  • Family history: Degree of relativity of the family member with breast cancer affects individual risk. For example, the relative risk of patients with an affected first-degree relative is 1.5-2 times higher when compared to controls without affected family members. Even more significantly, having two first-degree relatives affected (female or male) increases relative risk by more than 4-6 times when compared to patients without this risk factor. Third, age of the affected relative at time of diagnosis also influences risk. A patient with a mother diagnosed when younger than 60 years is at 2 times increased risk. Finally, bilateral cancer in a first-degree relative may increase risk by more than 6 times.
  • Genetic predisposition: Approximately 5-10% of breast cancer cases are primarily attributable to inherited factors. Claus et al estimated that 36% of breast cancer cases in women aged 20-29 years can be attributed to a single dominant susceptibility gene, while only 1% of women diagnosed with breast cancer over the age of 80 have such a gene. The risk of breast cancer in carriers of BRCA1 mutation is estimated to be 36-87%. Male breast cancer is also seen with BRCA1 mutations with a lifetime risk of 1-3%. Lifetime breast cancer risk for carriers of BRCA2 is 45-84%. BRCA2 mutations are associated with a 6% lifetime risk of male breast cancer. Genetic breast cancer syndromes are outlined in Table 1.

Table 1. Genetic Breast Cancer Syndromes.

Open table in new window

[ CLOSE WINDOW ]
Table
SyndromeGeneInheritanceCancersOther Features
Breast/ovarianBRCA1AD*Breast, ovarian
Cancer syndromeBRCA2ADBreast, ovarian, prostate, pancreaticFanconi anemia in homozygotes
Li-Fraumeni syndromeTP53ADBreast, brain, soft tissue sarcomas, leukemia, adrenocortical, others
Cowden diseasePTENADBreast, ovary, follicular thyroid, colonAdenomas of thyroid, fibroids, GI polyps
Peutz-Jegher syndromeSTKII/LKB1ADGI, breastHamartomas of bowel, pigmentation of buccal mucosa
Ataxia-telangiectasiaATMADBreastHomozygotes: leukemia, lymphoma, cerebella ataxia, immune deficiency, telangiectasias
Site-specificCHEK2ADBreastLow penetrance
Muir-Torre syndromeMSH2/MLH1ADColorectal, breast
SyndromeGeneInheritanceCancersOther Features
Breast/ovarianBRCA1AD*Breast, ovarian
Cancer syndromeBRCA2ADBreast, ovarian, prostate, pancreaticFanconi anemia in homozygotes
Li-Fraumeni syndromeTP53ADBreast, brain, soft tissue sarcomas, leukemia, adrenocortical, others
Cowden diseasePTENADBreast, ovary, follicular thyroid, colonAdenomas of thyroid, fibroids, GI polyps
Peutz-Jegher syndromeSTKII/LKB1ADGI, breastHamartomas of bowel, pigmentation of buccal mucosa
Ataxia-telangiectasiaATMADBreastHomozygotes: leukemia, lymphoma, cerebella ataxia, immune deficiency, telangiectasias
Site-specificCHEK2ADBreastLow penetrance
Muir-Torre syndromeMSH2/MLH1ADColorectal, breast
*AD = autosomal dominant

More controversial risk factors include obesity, low-dose radiation, and oral contraceptive use. The Breast Cancer Detection Demonstration Project (BCDDP) defined several factors not associated with increased risk, including oral contraceptive use, long-term (>15 y) menopausal estrogen use, modest alcohol use, and cigarette smoking. Various analyses of data from the Nurses’ Health Study also have shown no association between oral contraceptive use and breast cancer. Conflicting data preclude the recommendation of guidelines for risk modification in these areas.

Pathophysiology

The World Health Organization classification of breast tumors organizes both benign and malignant lesions by histologic pattern. Epithelial tumors comprise the largest group, including intraductal papilloma, adenomas, intraductal and lobular carcinoma in situ, invasive (ductal and lobular) carcinoma, and Paget disease of the nipple. Invasive ductal carcinoma is by far the most common type.

Phyllodes tumor, benign and malignant, and carcinosarcoma are rare lesions grouped as mixed connective tissue and epithelial tumors. Other common nonadenocarcinoma lesions of the breast include angiosarcoma and primary lymphoma.

Invasiveness is a key determinant in the prognosis and treatment of breast malignancy. Noninvasive lesions are by definition limited by the basement membrane and may be classified as DCIS or LCIS.

  • DCIS is by far more common than LCIS, and more importantly, it should be distinguished as a clearly malignant lesion. Ductal epithelial cells undergo malignant transformation and proliferate intraluminally. Eventually, the cells outstrip their blood supply and become necrotic centrally. This debris can calcify and be detected mammographically. Moreover, the lesions also may be palpable clinically. Five pathologic subtypes have been identified: comedo, papillary, micropapillary, solid, and cribriform. Most lesions represent a combination of at least two of these subtypes. The presence of comedo necrosis is an independent risk factor for subsequent ipsilateral breast cancer (NSABP-B17).
  • LCIS also arises from epithelial cells; however, their growth continues in a lobular pattern. In contrast to DCIS, these lesions rarely develop central necrosis, calcify, or become palpable. For this reason, LCIS rarely is detected by examination or mammography preoperatively and usually presents as an incidental finding on histologic review. Clinically, LCIS is considered more of a marker for development of invasive cancer rather than a malignant lesion. The risk of subsequent breast cancer is equal for both breasts irrespective of the index site. Moreover, most invasive cancers that develop are infiltrating ductal, which supports the concept that LCIS is not a malignant lesion.
  • Invasive breast cancers usually are epithelial tumors of ductal or lobular origin. Features such as size, status of surgical margin, estrogen receptors (ER) and progesterone receptors (PR), nuclear and histologic grade, DNA content, S-phase fraction, vascular invasion, tumor necrosis, and quantity of intraductal component are all important in deciding on a course of treatment for any breast tumor.
  • Infiltrating ductal carcinoma is the most commonly diagnosed breast tumor. This lesion, which accounts for 75% of breast cancers, has no specific histologic characteristics other than invasion through the basement membrane. DCIS may be a frequently associated finding on pathologic examination. It also has a tendency to metastasize via lymphatics.
  • Infiltrating lobular carcinoma has a much lower incidence and comprises less than 15% of invasive breast cancer. It is characterized histologically by the Indian file arrangement of small tumor cells. Like ductal carcinoma, these typically metastasize to axillary lymph nodes first. However, it also has a tendency to be more multifocal. Despite this, the prognosis is comparable to that of ductal carcinoma.

Less common histologic subtypes of adenocarcinoma collectively comprise less than 25% of invasive breast cancers.

  • The diagnosis of tubular carcinoma requires the presence of tubular formation in at least 75% of the specimen. This pathology is associated with improved prognosis.
  • Mucinous (or colloid) carcinoma also has a favorable prognosis when compared with ductal carcinoma. These slow-growing lesions characteristically produce large amounts of mucin, thus are usually bulky. They, like tubular carcinoma, rarely metastasize.
  • Medullary carcinoma, despite being a poorly differentiated tumor, also carries an improved prognosis.

ER and PR are valuable as predictors of disease-free survival and response to hormonal therapy. Studies in patients with ER(+) tumors who did not receive chemotherapy suggest they have a higher rate of disease-free survival than patients with ER(-) tumors. The presence of these nuclear steroid receptors on tumor staining should be considered, along with other histologic features, in determining the need for hormonal and adjuvant chemotherapy.

Human epidermal growth factor receptor (Her)-2/neu protein expression is associated with increased incidence of recurrence and shortened overall survival. Her-2/neu is overexpressed in 20-30% of breast cancers. Her-2/neu–positive lesions have also been associated with comedo-type DCIS, another poor prognostic indicator. Patients with Her-2/neu–positive breast cancer are candidates for treatment with combination chemotherapy and monoclonal antibody therapy.

Other histologic factors, such as lymphatic invasion, an extensive DCIS component (>25% of the tumor), and Ki-67 staining, continue to be investigated as potential prognostic factors for breast cancer.

Presentation

When evaluating a patient with possible breast cancer, direct questions toward both assessment of risk and narrowing the differential diagnosis. Patient factors associated with increased risk of breast cancer are discussed in Etiology. In addition, inquiry regarding nipple discharge, fever, pain, rapid growth, duration of the mass, and changes with menses may be helpful in directing the workup for breast cancer.

Physical examination should include inspection of the patient in the upright as well as supine positions. With the patient upright, assessment for symmetry and changes in the nipple and skin may be performed. Obvious size discrepancy, nipple inversion, skin dimpling, scaling, and edema (peau d'orange) are suggestive findings. Supraclavicular, infraclavicular, and axillary lymphadenopathy also can be best detected in this position.

Once the patient is in the supine position with the ipsilateral arm extended over the head, the breast parenchyma can be compressed against the chest wall, which allows for improved sensitivity for the examiner. The 2 most common techniques for supine examination are the clockwise radial pattern and the linear pattern. In the clockwise radial technique, examination begins at the 12-o'clock position near the clavicle and proceeds towards the nipple. This is repeated in a clockwise fashion around the entire breast.

The linear technique, when performed correctly, is arguably more sensitive, although time-consuming. Proponents of the linear technique recommend beginning in the axilla at the mid-axillary line, proceeding toward the inferior mammary fold, and then returning to the clavicle in a series of rows (12-15 rows, depending on the size of the breast). Using the pads of 3 fingertips, the examiner should palpate dime-sized circles in 3 different depths at each site before moving one finger width toward the inferior mammary fold and repeating the circular motion at the superficial, medium, and deep levels. Benign lesions are more frequently smaller, rubbery, well-circumscribed, and mobile. Characteristics suggestive of malignancy include skin involvement, fixation to the chest wall, irregular border, firmness, and enlargement.

Compression of the breast or nipple is no longer recommended to assess for discharge. However, visual inspection of the nipple/areola complex should be a routine part of the examination. Only spontaneous discharge should be considered clinically significant. Concerning characteristics include unilateral discharge, nonmilky fluid, and origin from a single duct. Intraductal papilloma, a benign finding, is the most common cause of unilateral bloody nipple discharge. Other benign pathology associated with nipple discharge includes subareolar duct ectasia and fibrocystic changes. Usually, malignant pathology presenting with nipple discharge is also associated with a palpable mass, suggestive mammographic findings, or both.

Breast self-examination, performed monthly, is still generally recommended for women beginning at age 18 years, although no strong statistical data exist to support its efficacy in the early detection of breast cancer. Physicians should examine patients aged 19-40 years approximately every 3 years. The American Cancer Society recommends annual evaluation by physician examination along with screening mammography for women aged 40 years and older, particularly if risk factors are present.

Relevant Anatomy

A thorough understanding of the relative anatomy of the breast and axilla is essential to successful and uncomplicated surgical treatment of breast cancer.

The breast is bounded by the clavicle superiorly, the sternum medially, the lateral border of the latissimus muscle laterally, and the inframammary fold inferiorly. The axillary tail of Spence extends into the deep fascia superior and lateral to the breast. The deep pectoral fascia defines the deep margin.

Fibrous bands, known as the suspensory ligaments of Cooper, divide the breast parenchyma into 12-20 separate lobules of glandular tissue. Separate branching lactiferous ducts drain each lobule. These ducts converge just beneath the nipple into sinuses that empty into a single terminal duct. Drainage from individual ducts can be localized for surgical excision.

The lateral pectoral nerve passes medially around the medial pectoralis minor, and the medial pectoral nerve passes laterally around the pectoralis minor. The names are based on the origin of the nerves from the lateral and medial cords of the brachial plexus rather than their orientation to the muscle. Injuries to these nerves are rare.

Injury to the brachial plexus can be avoided by keeping the superior extent of the axillary dissection inferior to the lower border of the axillary vein.

The thoracodorsal nerve is identifiable medial to the thoracodorsal vein running along to enter the latissimus dorsi. Injury may result in slight, if any, clinically evident weakening of the latissimus.

The long thoracic nerve is located more medially in the axilla. It runs just beneath the investing fascia of the serratus anterior, medial to the thoracodorsal complex. Injury to this nerve results in winging of the scapula on arm extension.

The skin of the axilla and upper arm is supplied by the intercostobrachial nerve, which often is sacrificed in the dissection of axillary nodes. Transection may result in numbness in these areas.

Axillary lymph nodes receive most mammary lymphatic drainage. The internal mammary nodes also receive some drainage medially. Axillary nodes are referred to by levels, which are defined by the pectoralis minor muscle. Level I nodes are lateral, II behind, and III medial to the muscle.

The external mammary artery and perforators of the internal mammary artery supply blood to the breast. Venous drainage follows arterial anatomy.

Contraindications

Contraindications to surgical resection depend on the procedure in question. Breast conservation therapy is applicable in most patients with early stage invasive carcinoma. Relative contraindications include small breast size, large tumor size (>5 cm), and collagen vascular disease. Absolute contraindications include multi-focal disease, history of prior radiation to the area of treatment, first or second trimester of pregnancy, and persistent positive margins following attempts at conservation.

Factors that often are considered but should not be absolute deterrents include axillary node involvement and tumor location. Consideration of cosmesis, while important, should never outweigh the clinical priority of obtaining negative surgical margins. For example, lesions involving Paget's disease of the nipple may be treated with excision of the nipple-areolar complex and reconstruction. Larger lesions in patients with concerns regarding cosmesis may be better served by standard modified radical mastectomy and immediate reconstruction.

A relative contraindication to modified radical mastectomy is locally advanced cancer requiring neo-adjuvant therapy prior to surgical intervention.

More on Breast Cancer

Overview: Breast Cancer
Workup: Breast Cancer
Treatment: Breast Cancer
Follow-up: Breast Cancer
Multimedia: Breast Cancer
References
[ CLOSE WINDOW ]

References

  1. Fisher B, Bauer M, Margolese R, et al. Five-year results of a randomized clinical trial comparing total mastectomy and segmental mastectomy with or without radiation in the treatment of breast cancer. N Engl J Med. Mar 14 1985;312(11):665-73. [Medline].

  2. Hortobagyi GN, de la Garza Salazar J, Pritchard K, et al. The global breast cancer burden: variations in epidemiology and survival. Clin Breast Cancer. Dec 2005;6(5):391-401. [Medline].

  3. American Cancer Society. Breast Cancer Facts & Figures 2007-2008. Atlanta, Ga: American Cancer Society, Inc.; [Full Text].

  4. Colditz GA, Hankinson SE, Hunter DJ, et al. The use of estrogens and progestins and the risk of breast cancer in postmenopausal women. N Engl J Med. Jun 15 1995;332(24):1589-93. [Medline].

  5. Bear HD, Anderson S, Brown A, et al. The effect on tumor response of adding sequential preoperative docetaxel to preoperative doxorubicin and cyclophosphamide: preliminary results from National Surgical Adjuvant Breast and Bowel Project Protocol B-27. J Clin Oncol. Nov 15 2003;21(22):4165-74. [Medline].

  6. Kriege M, Brekelmans CT, Boetes C, et al. Efficacy of MRI and mammography for breast-cancer screening in women with a familial or genetic predisposition. N Engl J Med. Jul 29 2004;351(5):427-37. [Medline].

  7. Fisher B, Costantino JP, Wickerham DL, et al. Tamoxifen for prevention of breast cancer: report of the National Surgical Adjuvant Breast and Bowel Project P-1 Study. J Natl Cancer Inst. Sep 16 1998;90(18):1371-88. [Medline].

  8. National Surgical Adjuvant Breast Project (NSABP). Study of tamoxifen and raloxifene (STAR). NSABP Web site. Available at http://www.nsabp.pitt.edu/STAR/Index.asp. Accessed April 9, 2009.

  9. Vogel VG, Costantino JP, Wickerham DL, et al. Effects of tamoxifen vs raloxifene on the risk of developing invasive breast cancer and other disease outcomes: the NSABP Study of Tamoxifen and Raloxifene (STAR) P-2 trial. JAMA. Jun 21 2006;295(23):2727-41. [Medline].

  10. Romond EH, Perez EA, Bryant J, et al. Trastuzumab plus adjuvant chemotherapy for operable HER2-positive breast cancer. N Engl J Med. Oct 20 2005;353(16):1673-84. [Medline].

  11. Ravdin PM, Davis G. Adjuvant! Online Version 8.0. www.adjuvantonline.com. 2005;[Full Text].

  12. Lagios MD, Margolin FR, Westdahl PR, Rose MR. Mammographically detected duct carcinoma in situ. Frequency of local recurrence following tylectomy and prognostic effect of nuclear grade on local recurrence. Cancer. Feb 15 1989;63(4):618-24. [Medline].

  13. Silverstein MJ, Poller DN, Waisman JR, et al. Prognostic classification of breast ductal carcinoma-in-situ. Lancet. May 6 1995;345(8958):1154-7. [Medline].

  14. Silverstein MJ, Lagios MD, Craig PH, et al. A prognostic index for ductal carcinoma in situ of the breast. Cancer. Jun 1 1996;77(11):2267-74. [Medline].

  15. Fisher ER, Dignam J, Tan-Chiu E, et al. Pathologic findings from the National Surgical Adjuvant Breast Project (NSABP) eight-year update of Protocol B-17: intraductal carcinoma. Cancer. Aug 1 1999;86(3):429-38. [Medline].

  16. Haagensen CD, Lane N, Lattes R, Bodian C. Lobular neoplasia (so-called lobular carcinoma in situ) of the breast. Cancer. Aug 1978;42(2):737-69. [Medline].

  17. Veronesi U, Saccozzi R, Del Vecchio M, et al. Comparing radical mastectomy with quadrantectomy, axillary dissection, and radiotherapy in patients with small cancers of the breast. N Engl J Med. Jul 2 1981;305(1):6-11. [Medline].

  18. Krag D, Weaver D, Ashikaga T, et al. The sentinel node in breast cancer--a multicenter validation study. N Engl J Med. Oct 1 1998;339(14):941-6. [Medline].

  19. Giuliano AE, Haigh PI, Brennan MB, et al. Prospective observational study of sentinel lymphadenectomy without further axillary dissection in patients with sentinel node-negative breast cancer. J Clin Oncol. Jul 2000;18(13):2553-9. [Medline].

  20. Cox CE, Bass SS, Boulware D, et al. Implementation of new surgical technology: outcome measures for lymphatic mapping of breast carcinoma. Ann Surg Oncol. Sep 1999;6(6):553-61. [Medline].

  21. Cox CE, Nguyen K, Gray RJ, et al. Importance of lymphatic mapping in ductal carcinoma in situ (DCIS): why map DCIS?. Am Surg. Jun 2001;67(6):513-9; discussion 519-21. [Medline].

  22. Nabholtz JM, Slamon D. New adjuvant strategies for breast cancer: meeting the challenge of integrating chemotherapy and trastuzumab (Herceptin). Semin Oncol. Feb 2001;28(1 Suppl 3):1-12. [Medline].

  23. National Cancer Institute. Personalized Treatment Trial for Breast Cancer Launched. www.cancer.gov. Available at www.cancer.gov/newscenter/pressreleases/TAILORxRelease. Accessed June 3, 2009.

  24. American Cancer Society. Breast Cancer Facts & Figures 2006. American Cancer Society. 2006.

  25. Colditz, GA. Recent Advances and Future Directions in Endocrine Manipulation of Breast Cancer. Clinical Cancer Research. 2005;11:909s-917s.

  26. Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and hormone replacement therapy: collaborative reanalysis of data from 51 epidemiological studies of 52,705 women with breast cancer and 108,411 women without breast cancer. Lancet. Oct 11 1997;350(9084):1047-59. [Medline].

  27. Cote RJ, Peterson HF, Chaiwun B, et al. Role of immunohistochemical detection of lymph-node metastases in management of breast cancer. International Breast Cancer Study Group. Lancet. Sep 11 1999;354(9182):896-900. [Medline].

  28. Daling JR, Malone KE, Doody DR, et al. Relation of regimens of combined hormone replacement therapy to lobular, ductal, and other histologic types of breast carcinoma. Cancer. Dec 15 2002;95(12):2455-64. [Medline].

  29. Davidson NE, Morrow M, Kopans DB, Koerner FC. Case records of the Massachusetts General Hospital. Case 35-2005. A 56-year-old woman with breast cancer and isolated tumor cells in a sentinel lymph node. N Engl J Med. Nov 17 2005;353(20):2177-85. [Medline].

  30. Easton DF, Ford D, Bishop DT. Breast and ovarian cancer incidence in BRCA1-mutation carriers. Breast Cancer Linkage Consortium. Am J Hum Genet. Jan 1995;56(1):265-71. [Medline].

  31. Fisher B, Bryant J, Wolmark N, et al. Effect of preoperative chemotherapy on the outcome of women with operable breast cancer. J Clin Oncol. Aug 1998;16(8):2672-85. [Medline].

  32. Fisher B, Costantino J. Highlights of the NSABP Breast Cancer Prevention Trial. Cancer Control. Jan 1997;4(1):78-86. [Medline].

  33. Fisher B, Dignam J, Tan-Chiu E, et al. Prognosis and treatment of patients with breast tumors of one centimeter or less and negative axillary lymph nodes. J Natl Cancer Inst. Jan 17 2001;93(2):112-20. [Medline].

  34. Fisher B, Redmond C, Fisher ER, et al. Ten-year results of a randomized clinical trial comparing radical mastectomy and total mastectomy with or without radiation. N Engl J Med. Mar 14 1985;312(11):674-81. [Medline].

  35. Gail MH, Costantino JP, Bryant J, et al. Weighing the risks and benefits of tamoxifen treatment for preventing breast cancer. J Natl Cancer Inst. Nov 3 1999;91(21):1829-46. [Medline].

  36. Gann PH, Colilla SA, Gapstur SM, et al. Factors associated with axillary lymph node metastasis from breast carcinoma: descriptive and predictive analyses. Cancer. Oct 15 1999;86(8):1511-9. [Medline].

  37. Greenlee RT, Murray T, Bolden S, Wingo PA. Cancer statistics, 2000. CA Cancer J Clin. Jan-Feb 2000;50(1):7-33. [Medline].

  38. Haffty BG, Harrold E, Khan AJ, et al. Outcome of conservatively managed early-onset breast cancer by BRCA1/2 status. Lancet. Apr 27 2002;359(9316):1471-7. [Medline].

  39. Harris JR, Lippman ME, Veronesi U, Willett W. Breast cancer (1). N Engl J Med. Jul 30 1992;327(5):319-28. [Medline].

  40. Harris JR, Lippman ME, Veronesi U, Willett W. Breast cancer (2). N Engl J Med. Aug 6 1992;327(6):390-8. [Medline].

  41. Harris JR, Lippman ME, Veronesi U, Willett W. Breast cancer (3). N Engl J Med. Aug 13 1992;327(7):473-80. [Medline].

  42. Kopans DB, Meyer JE, Sadowsky N. Breast imaging. N Engl J Med. Apr 12 1984;310(15):960-7. [Medline].

  43. Kuerer HM, Hunt KK, Newman LA, et al. Neoadjuvant chemotherapy in women with invasive breast carcinoma: conceptual basis and fundamental surgical issues. J Am Coll Surg. Mar 2000;190(3):350-63. [Medline].

  44. Kuerer HM, Newman LA, Smith TL, et al. Clinical course of breast cancer patients with complete pathologic primary tumor and axillary lymph node response to doxorubicin-based neoadjuvant chemotherapy. J Clin Oncol. Feb 1999;17(2):460-9. [Medline].

  45. Lee CH, Egglin TK, Philpotts L, et al. Cost-effectiveness of stereotactic core needle biopsy: analysis by means of mammographic findings. Radiology. Mar 1997;202(3):849-54. [Medline].

  46. Li CI, Malone KE, Porter PL, et al. Relationship between long durations and different regimens of hormone therapy and risk of breast cancer. JAMA. Jun 25 2003;289(24):3254-63. [Medline].

  47. Lippman ME, Krueger KA, Eckert S, et al. Indicators of lifetime estrogen exposure: effect on breast cancer incidence and interaction with raloxifene therapy in the multiple outcomes of raloxifene evaluation study participants. J Clin Oncol. Jun 15 2001;19(12):3111-6. [Medline].

  48. Madigan MP, Ziegler RG, Benichou J, et al. Proportion of breast cancer cases in the United States explained by well-established risk factors. J Natl Cancer Inst. Nov 15 1995;87(22):1681-5. [Medline].

  49. Mamounas EP. NSABP Protocol B-27. Preoperative doxorubicin plus cyclophosphamide followed by preoperative or postoperative docetaxel. Oncology (Williston Park). Jun 1997;11(6 Suppl 6):37-40. [Medline].

  50. Mamounas EP, Brown A, Anderson S, et al. Sentinel node biopsy after neoadjuvant chemotherapy in breast cancer: results from National Surgical Adjuvant Breast and Bowel Project Protocol B-27. J Clin Oncol. Apr 20 2005;23(12):2694-702. [Medline].

  51. Margolese R, Poisson R, Shibata H, et al. The technique of segmental mastectomy (lumpectomy) and axillary dissection: A syllabus from the National Surgical Adjuvant Breast Project workshops. Surgery. Nov 1987;102(5):828-34. [Medline].

  52. Martin AM, Weber BL. Genetic and hormonal risk factors in breast cancer. J Natl Cancer Inst. Jul 19 2000;92(14):1126-35. [Medline].

  53. Mauri D, Pavlidis N, Ioannidis JP. Neoadjuvant versus adjuvant systemic treatment in breast cancer: a meta-analysis. J Natl Cancer Inst. Feb 2 2005;97(3):188-94. [Medline].

  54. McMasters KM, Tuttle TM, Carlson DJ, et al. Sentinel lymph node biopsy for breast cancer: a suitable alternative to routine axillary dissection in multi-institutional practice when optimal technique is used. J Clin Oncol. Jul 2000;18(13):2560-6. [Medline].

  55. Morrow M, Harris J. Ductal Carcinoma In Situ and Microinvasive Carcinoma. Diseases of the Breast, 3rd ed. 2004;521-537.

  56. Morrow M, Schnitt SJ. Treatment selection in ductal carcinoma in situ. JAMA. Jan 26 2000;283(4):453-5. [Medline].

  57. O'Shaughnessy J. Extending survival with chemotherapy in metastatic breast cancer. Oncologist. 2005;10 Suppl 3:20-9. [Medline].

  58. Paik S, Shak S, Tang G, et al. A multigene assay to predict recurrence of tamoxifen-treated, node-negative breast cancer. N Engl J Med. Dec 30 2004;351(27):2817-26. [Medline].

  59. Pierce L. Radiotherapy for breast cancer in BRCA1/BRCA2 carriers: clinical issues and management dilemmas. Semin Radiat Oncol. Oct 2002;12(4):352-61. [Medline].

  60. Singletary SE, Allred C, Ashley P, et al. Revision of the American Joint Committee on Cancer staging system for breast cancer. J Clin Oncol. Sep 1 2002;20(17):3628-36. [Medline].

  61. Slamon DJ, Leyland-Jones B, Shak S, et al. Use of chemotherapy plus a monoclonal antibody against HER2 for metastatic breast cancer that overexpresses HER2. N Engl J Med. Mar 15 2001;344(11):783-92. [Medline].

  62. Smart CR, Byrne C, Smith RA, et al. Twenty-year follow-up of the breast cancers diagnosed during the Breast Cancer Detection Demonstration Project. CA Cancer J Clin. May-Jun 1997;47(3):134-49. [Medline].

  63. Tormey SM, Malone CM, McDermott EW. Current status of combined hormone replacement therapy in clinical practice. Clinical Breast Cancer. 2006;Feb (6 Suppl 2):S51-7. [Medline].

  64. Van Zee KJ, Manasseh DM, Bevilacqua JL, et al. A nomogram for predicting the likelihood of additional nodal metastases in breast cancer patients with a positive sentinel node biopsy. Ann Surg Oncol. Dec 2003;10(10):1140-51. [Medline].

  65. Veronesi U. Conservative treatment of breast cancer: a trial in progress at the Cancer Institute of Milan. World J Surg. May 1977;1(3):324-6. [Medline].

  66. Veronesi U, Zucali R, Del Vecchio M. Conservative treatment of breast cancer with QU.A.R.T. Technique. World J Surg. Oct 1985;9(5):676-81. [Medline].

  67. Warmuth MA, Sutton LM, Winer EP. A review of hereditary breast cancer: from screening to risk factor modification. Am J Med. Apr 1997;102(4):407-15. [Medline].

  68. Winchester DP, Jeske JM, Goldschmidt RA. The diagnosis and management of ductal carcinoma in-situ of the breast. CA Cancer J Clin. May-Jun 2000;50(3):184-200. [Medline].

  69. Wingo PA, Ries LA, Rosenberg HM, et al. Cancer incidence and mortality, 1973-1995: a report card for the U.S. Cancer. Mar 15 1998;82(6):1197-207. [Medline].

  70. Wolmark N, Wang J, Mamounas E, et al. Preoperative chemotherapy in patients with operable breast cancer: nine-year results from National Surgical Adjuvant Breast and Bowel Project B-18. J Natl Cancer Inst Monogr. 2001;96-102. [Medline].

  71. Wood WC, Skandalakis JE. Anatomic Basis of Tumor Surgery. 1st ed. Quality Medical Publishing;1999.

[ CLOSE WINDOW ]

Further Reading

[ CLOSE WINDOW ]

Keywords

breast cancer, mastectomy, radical mastectomy, lumpectomy, radiation therapy, XRT, breast cancer treatment, breast cancer causes, breast cancer symptoms, chemotherapy, benign lesions, malignant lesions, epithelial tumors, intraductal papilloma, adenoma, intraductal carcinoma, invasive carcinoma, Paget disease of the nipple

invasive ductal carcinoma, phyllodes tumor, carcinosarcoma, ductal carcinoma in situ, DCIS, lobular carcinoma in situ, LCIS, Li-Fraumeni syndrome, Muir-Torre syndrome, Cowden disease, Peutz-Jeghers syndrome, mutation, mutation, adenocarcinoma, tubular carcinoma, mucinous carcinoma, colloid carcinoma, mucin, medullary carcinoma, mammography, inflammatory breast cancer

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Mary Jo Wright, MD, Associate Professor of Surgery, Chief of Breast Surgery Service, Tulane University School of Medicine; Medical Director, Breast Cancer Center, Medical Center of Louisiana, New Orleans
Mary Jo Wright, MD is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Surgeons, American College of Surgeons, American Society of Breast Disease, American Society of Breast Surgeons, Association for Academic Surgery, Association for Surgical Education, Association of Women Surgeons, Eastern Association for the Surgery of Trauma, Orleans Parish Medical Society, Society of Critical Care Medicine, and Society of Surgical Oncology
Disclosure: Nothing to disclose.

Coauthor(s)

Krzysztof Moroz, MD, Professor of Pathology, Director of Cytopathology, Tulane University Health Sciences Center
Krzysztof Moroz, MD is a member of the following medical societies: American Society for Clinical Pathology, American Society of Cytopathology, College of American Pathologists, and United States and Canadian Academy of Pathology
Disclosure: Nothing to disclose.

R Edward Newsome, MD, Program Director and Chief of Plastic Surgery, Henderson Chair in Surgery, Assistant Dean for Graduate Medical Education, Tulane University School of Medicine
R Edward Newsome, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Society of Plastic and Reconstructive Surgery, American Society of Plastic Surgeons, and Louisiana State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Christian Paletta, MD, FACS, Professor, Division Chief and Program Director, Department of Plastic and Reconstructive Surgery, St Louis University School of Medicine
Christian Paletta, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American Association of Plastic Surgeons, American Burn Association, American Cleft Palate/Craniofacial Association, American College of Surgeons, American Medical Association, and Missouri State Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Saleh M Shenaq, MD†, Former Director and Founder, The International Brachial Plexus Institute; Former Chief, Section of Plastic Surgery, Methodist Hospital, Houston
Saleh M Shenaq, MD† is a member of the following medical societies: American Academy of Anti-Aging Medicine, American Academy of Pediatrics, American Association for Hand Surgery, American Association for the Advancement of Science, American Association of Plastic Surgeons, American Burn Association, American College of Physician Executives, American College of Surgeons, American Congress of Rehabilitation Medicine, American Medical Association, American Society for Aesthetic Plastic Surgery, American Society for Reconstructive Microsurgery, American Society for Surgery of the Hand, American Society of Gene Therapy, American Society of Law Medicine and Ethics, American Society of Maxillofacial Surgeons, American Society of Plastic Surgeons, American Trauma Society, Association for Academic Surgery, International College of Surgeons, Lipoplasty Society of North America, Plastic Surgery Research Council, Society for Neuroscience, Society of Surgical Oncology, Southern Medical Association, Texas Medical Association, and Texas Society of Plastic Surgeons
Disclosure: Nothing to disclose.

CME Editor

Nicolas (Nick) G Slenkovich, MD, Director, Colorado Plastic Surgery Center
Nicolas (Nick) G Slenkovich, MD is a member of the following medical societies: American Academy of Otolaryngology-Head and Neck Surgery, American College of Surgeons, American Medical Association, American Society of Aesthetic Plastic Surgery, American Society of Plastic Surgeons, and Colorado Medical Society
Disclosure: Nothing to disclose.

Chief Editor

James Neal Long, MD, Assistant Professor of Plastic and Reconstructive Surgery, Division of Plastic Surgery, University of Alabama at Birmingham and Kirklin Clinics
James Neal Long, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Medical Association, American Society of Plastic Surgeons, Plastic Surgery Research Council, Sigma Xi, Southeastern Society of Plastic and Reconstructive Surgeons, and Southeastern Surgical Congress
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.