Anatomy and Pathology
A basic knowledge of breast structure and development is essential to perform an effective clinical breast examination. Likewise, a familiarity with benign and malignant changes of the breast is necessary to understand breast cancer and its management.
The breast lies between the second and sixth ribs, from the sternal edge to the edge of the axilla, and against the pectoralis muscle on the chest wall. Breast tissue also projects into the axilla as the tail of Spence. For clinical purposes, the breast is divided into four quadrants: upper inner, upper outer, lower inner and lower outer quadrants. Cancer occurs most often in the upper outer quadrant.
The breast is composed of 15-20 lobes that are made up of many smaller lobules. The lobule (sometimes called the ductal-lobular unit) is the basic structural unit of the breast and is lined by epithelial cells. Each lobule is subdivided into 10 to 100 alveoli, the milk producing units of the breast. Milk flows from the alveoli of the lobules into ducts. The ducts gradually coalesce into major ducts that terminate in the nipple.
Breasts also contain blood and lymphatic vessels. Most lymphatic vessels within the breast lead to axillary lymph nodes. Some also connect to supra- or infraclavicular nodes and internal mammary nodes. Cancer cells may enter lymphatic vessels and spread to lymph nodes. Cancer cells may also enter blood vessels and spread to other parts of the body.
Beneath the tissues of the breast lie the muscles of the chest wall and between the two is the fascia (a layer of connective tissue). Two layers of suspensory ligaments (Cooper's ligaments) link the breast to the fascia, providing support. As these ligaments stretch with age or weight gain, the breast loses some of its firmness.
Breast tissue begins to develop around the sixth week in utero with the formation of the mammary ridge. Also called the mammary fold or milk line, this thickening of the skin extends from just below the axilla to the inguinal region (groin area). It then recedes before birth, leaving two primary breast buds on the upper half of the chest. In newborns, the nipples and beginnings of the milk duct system are present. This rudimentary system remains essentially at rest until puberty. For females, usually around the ages of 10 or 11, the release of ovary producing hormones (estrogen and progesterone) stimulates further development of the ducts and lobules. At the same time, increases in adipose tissue (fatty tissue) and fibrous connective tissue cause the breasts to enlarge. By adulthood, all glandular elements are fully formed and breast development is complete. At menopause, the lobules recede, leaving mostly ducts, adipose and fibrous tissue. Histologically, postmenopausal and prepubertal breasts are very similar.
Throughout a woman's life, breast tissue remains sensitive to hormonal changes.
Throughout a woman's life, breast tissue remains sensitive to hormonal changes, including those that occur during menstruation, pregnancy, and lactation. During each menstrual cycle, levels of estrogen and progesterone rise, causing ducts and milk glands to enlarge. In pregnancy, rising hormonal levels cause further branching and differentiation of the ducts and lobules, accompanied by an increase in adipose tissue and richer blood flow. With lactation, lobules become dilated and engorged with colostrum and milk. Lactation also increases the possibility of abnormal nipple discharge, infection, and inflammation, although nonlactating women may also experience these types of benign breast changes.
Benign changes of the breast are very common and can be found in most women.
Benign breast changes refer to a heterogeneous group of lesions that may present as a palpable mass or a nonpalpable abnormality found either through imaging tests or biopsy.1 Many lesions appear similar to breast cancer, yet the vast majority of lumps, inflammations, nipple discharges, and other breast changes are not cancerous. Benign changes of the breast are very common and can be found in most women.2 3
Benign breast changes are usually categorized into three descriptive subtypes based upon the appearance of tissue cells under a microscope: (1) nonproliferative lesions; (2) proliferative lesions without atypia; and (3) atypical hyperplasias.1 The relative risk of developing into subsequent breast cancer is different for each subtype.
Benign Breast Changes:
- Nonproliferative Lesions
- • Cysts
- • Papillary apocrine change
- • Epithelial-related calcifications
- • Mild hyperplasia of the usual type
- Proliferative Lesions without Atypia
- • Usual ductal hyperplasia
- • Intraductal papillomas
- • Radial scars
- • Sclerosing adenosis
- • Fibroadenomas (simple and complex)
- Atypical Hyperplasias
- • Atypical ductal hyperplasia
- • Atypical lobular hyperplasia
- • Flat epithelial atypia
Nonproliferative lesions include cysts, papillary apocrine change, epithelial-related calcifications, and mild hyperplasia of the usual type.1 In women with nonproliferative breast lesions, the risk of subsequent breast cancer is about the same as that of the general population but may be slightly elevated in some women with a strong family history of breast cancer.1 4 5 6
Proliferative lesions without atypia are characterized by excessive cell growth, especially of the duct linings, but with no cells appearing abnormal. These lesions include usual ductal hyperplasia (also known as moderate or florid hyperplasia of the usual type), intraductal papillomas, radial scars, sclerosing adenosis, and fibroadenomas (both simple and complex).1 Most proliferative breast lesions without atypia are associated with a slightly elevated risk of developing invasive breast cancer - approximately 1.5 to 2.0 times that of the general population.1 5 However, for the majority of women with simple fibroadenomas, there is no increased risk; risk is elevated only if the fibroadenoma is complex or accompanied by adjacent proliferative disease or if the woman has a family history of breast cancer.4
Atypical hyperplasias include atypical ductal hyperplasia (ADH) and atypical lobular hyperplasia (ALH). ADH and ALH have some, but not all, of the characteristics of carcinoma in situ and are characterized by excessive cell growth with some cells appearing abnormal. ADH and ALH carry an approximate 3.5 to 5.0 times increase in the relative risk of developing breast cancer. The highest relative risk appears to be from ALH that involves both lobules and ducts.1 4 7 8
In addition to ADH and ALH, the term flat epithelia atypia (FEA) is a categorization proposed by the World Health Organization to encompass the terms columnar cell change with atypia, columnar cell hyperplasia with atypia, and clinging carcinoma of the monomorphic type. FEA features dilated ducts that are lined by atypical columnar epithelial cells. It may be a precursor to or an early manifestation of ductal carcinoma in situ (DCIS). Current research suggests that the risk of progression of FEA to invasive breast cancer is low.1 4 7
Benign breast lesions are usually confirmed by imaging tests and/or biopsy. Thus, every irregularity should be brought to the attention of a healthcare provider for conclusive diagnosis. Whether or not treatment is required depends upon a number of factors including the exact nature of the diagnosis, a woman's discomfort, impact on future imaging, and the potential of the lesion for developing into breast cancer.2 4
Lobular Carcinoma In Situ (LCIS)
Lobular carcinoma in situ (LCIS) is an indolent, non-invasive breast lesion characterized by abnormal changes in the cells that line the milk-producing lobules and ducts of the breast. Despite its name, LCIS is not an in situ cancer. Rather, LCIS is a marker indicating that a woman is at increased risk of developing breast cancer. Compared to women without LCIS, women with this diagnosis have a 7 to 10 times higher risk of developing breast cancer. Risk increases by about 1% per year after diagnosis and remains steady over a woman's lifetime. However, most women with LCIS will never develop breast cancer. It is currently impossible to predict which women will and will not. 9 10
LCIS is often multifocal and may be bilateral in up to one-third of cases. Since there are rarely clinical or mammographic signs, it is almost always discovered as an incidental finding from a breast biopsy.9 LCIS occurs primarily in pre-menopausal women between 40-55 years old.9 11 LCIS is usually positive for estrogen and progesterone receptors and negative for the overexpression of the oncogene human epidermal growth factor receptor 2, HER-2/neu (also known as HER2).9 10
Lobular carcinoma in situ and atypical lobular hyperplasia have many similar features and are sometimes grouped together and termed "lobular neoplasia" (LN). LN is used to describe a spectrum of non-invasive, proliferative, atypical lesions that originate in the terminal ductal-lobular units (TDLU) of the breast.9 Because the relative risk of invasive breast cancer is much higher with lobular carcinoma in situ than atypical lobular hyperplasia, their distinction may be important in determining the course of treatment.7 11
Pleomorphic LCIS (PLCIS) is a variant of LCIS that consists of larger and more deranged cells. PLCIS is more likely than LCIS to be negative for estrogen and progesterone receptors and positive for HER2 overexpression. The features of PLCIS are similar to ductal carcinoma in situ (DCIS). DCIS requires a more aggressive treatment approach than PCLIS. A differential diagnosis is important in order to avoid overtreatment.9
Cancer is a process in which normal cells eventually change to abnormal cells that multiply out of control. Many breast cancers arise from a sequence that begins with an increase in the number of breast cells (hyperplasia) to the emergence of atypical breast cells (atypical hyperplasia) followed by carcinoma in situ (noninvasive cancer) and finally, invasive cancer. However, not all breast cancers necessarily follow this progressive pattern, and the speed of progression for those that do is highly variable. In addition, some cancers may never progress beyond in situ disease.
Breast cancer cell, photographed by
a scanning electron microscope.
Ductal carcinoma in situ (DCIS), also known as stage 0 breast cancer, accounts for roughly 20-25% of newly diagnosed breast cancer cases in the United States.12 DCIS refers to a broad spectrum of proliferative lesions in the breast duct. Some women with DCIS will develop invasive breast cancer, but it is not yet possible to identify which women will develop invasive breast cancer after a DCIS diagnosis.13 14 Factors that may influence the risk of invasion include nuclear grade of the tumor and presence and extent of necrosis. High-grade DCIS and comedo-type necrosis are highly correlated with recurrence and the development of invasive carcinoma. With early detection and treatment, the ten-year survival rate for DCIS is 96-98%.13 14
DCIS most often occurs at a single site.12 13 In the majority of cases (90%), DCIS is not palpable and is discovered through screening mammography as calcifications.12 13 DCIS is more commonly diagnosed in older women with the incidence rising steadily after age 40. Low grade DCIS is typically positive for estrogen (ER) and progesterone receptors (PR) and negative for the overexpression of HER2. High grade DCIS is estrogen positive in 30-90% of cases and shows variability in the presence of progesterone receptors. Seventy percent of high and intermediate grade DCIS are positive for HER2 amplification.12
DCIS is classified in at least two ways. It is often divided into subcategories based upon its growth pattern and architectural features. These subtypes include (1) solid; (2) cribriform; (3) micropapillary; and (4) papillary. There are also special types of DCIS, such as apocrine, neuroendocrine, clinging, intraductal signet ring carcinoma, hypersecretory duct carcinoma, and clear cell carcinoma. Intracystic papillary carcinoma and solid-papillary DICS are additional special variants.15 16 DCIS with mixed architectural patterns is most frequent, making up 62% of cases, followed by DCIS of the solid subtype (31%).12
DCIS is also commonly classified into subtypes based on nuclear grade, extent of necrosis, and architectural type.12 Certain features of DCIS, such as nuclear grade, necrosis, polarization, and architectural patterns, should be routinely documented in the pathology report.17 18
Invasive Breast Carcinoma
Invasive ductal carcinoma is the
most common type of breast cancer.
Invasive ductal carcinoma (IDC) is the most common type of breast cancer, accounting for 70-80% of invasive breast cancers.19 20 It is often called infiltrating ductal carcinoma, or infiltrating/invasive ductal carcinoma not otherwise specified (NOS) or of no special type (NST).
Histology: Breast Cancer
The cancer cells have penetrated the basement membrane that separates the ductal epithelium from the underlying tissue and invaded the surrounding breast tissue. The cells may then metastasize to other parts of the body through the bloodstream or lymphatic system. The prognosis for IDC depends upon many factors, including tumor morphology, histologic grade, hormone receptor status (estrogen and progesterone), HER2 expression, patterns of gene expression, and lymphovascular invasion.21
(See also Diagnosis and Staging, Pathology and Prognostic Factors
IDC may present as a palpable mass or may be found on screening mammography. The risk of developing IDC increases with age.22 Approximately 70-80% of IDC is positive for estrogen receptors; HER2 is overexpressed in about 15% of IDC cases.21
IDC is commonly classified into subtypes based upon its histological grade: (1) Grade 1/well differentiated; (2) Grade 2/moderately differentiated; and (3) Grade 3/poorly differentiated. In general, a lower grade is associated with a more favorable prognosis.21
Invasive lobular carcinoma (ILC) is relatively uncommon, comprising about 5-15% of invasive breast cancers. While some experts contend that the prognosis is similar to that of invasive ductal carcinoma, others suggest the prognosis for ILC is more favorable, at least in the short term. ILC tends to metastasize later than invasive ductal carcinoma.15 21
Compared with invasive ductal carcinoma, patients with ILC are more often prone to bilateral disease and the tumors tend to be multicentric, larger, and better differentiated. Because of its infiltrative growth pattern, a diagnosis of ILC may be challenging, particularly with dense breast tissue. ILC may present as a poorly defined mass or palpable thickening. Mammographic findings are often subtle, and often there is no focal mass or cluster microcalcifications. Ultrasound may assist in delineating lesions.23 ILC tends to occur later in life than invasive ductal carcinoma.24 It is most often estrogen and progesterone receptor positive and negative for HER2 overexpression. In one study, ILC was estrogen receptor positive in 93% of cases, progesterone receptor positive in 60% of cases, and HER2 positive in fewer than 1% of cases.25 It is difficult to obtain clear margins during surgery for ILC. 15 21
Other, less common, breast carcinomas include: (1) tubular; (2) mucinous; (3) medullary; (4) invasive cribriform; (5) invasive papillary; (6) invasive mircopapillary; (7) metaplastic; (8) neuroendocrine; (9) adenoid cystic; (10) apocrine; (11) secretory; (12) invasive carcinoma with osteoclast-like giant cells; (13) invasive carcinoma with choriocarcinomatous features; (14) lipid-rich and glycogen-rich carcinomas; and (15) mucinous cystadenocarcinoma. These carcinomas vary in their incidence, clinical presentation, age at diagnosis, biomarkers, and prognosis. 15 21 26 27
Other Types of Breast Cancer
Inflammatory breast cancer (IBC) is a rare, aggressive form of breast cancer, accounting for 1-5% of breast cancers.28 Nearly all cases of inflammatory breast cancer will have metastasized to the lymph nodes at the time of diagnosis, and approximately one-third will have metastasized to distant sites. The overall prognosis for this cancer is poor.28 29
Symptoms of IBC appear rapidly, typically within three months, and spread across at least one-third of the breast. Clinical features include breast enlargement, warmth, thickening or dimpling of hair follicles (peau d' orange), and ridges. Patients usually present without a palpable mass. IBC is usually unilateral. The mean age of diagnosis, 58, is younger than for other breast cancers. The majority of IBC cases are estrogen and progesterone receptor negative, and approximately 60% overexpress HER2. Patients whose IBC is estrogen and progesterone receptor negative have a less favorable prognosis, whereas HER2 expression does not appear to be prognostic.29
Paget disease of the nipple accounts for 1-3% of breast cancers and is associated with tumors inside the same breast in 85-88% of patients.30 Underlying tumors are most often invasive or in situ ductal carcinomas and are centrally located. The prognosis for Paget's disease depends largely on the characteristics of the underlying tumor. The prognosis is excellent when associated with carcinoma in situ.30 31 Patients presenting with a palpable mass usually have an underlying invasive carcinoma and metastases to the lymph nodes. The prognosis for these patients is poor. 32
The clinical presentation of Paget's disease may include erythema and scaling of the nipple skin, as well as nipple tingling, itching, increased sensitivity, burning, pain or oozing. About half of patients will also present with a palpable mass. The mean age of diagnosis is 62 years.30 31 Paget's cells are most often estrogen and progesterone receptor negative. They tend to be positive for the overexpression of HER2. 32 33
Phyllodes tumors (also spelled phylloides) are fibroepithelial lesions that demonstrate a wide range of biological behavior. These tumors account for less than one percent of all breast malignancies.34
Phyllodes tumors usually present as painless, palpable masses and often grow rapidly. The mass may bulge and may cause the breast skin to appear stretched and shiny. The mean age for diagnosis is in the 40s. The gross appearance of most phylloides tumors, particularly those that are benign, is not distinctly different from fibroadenomas. Most phyllodes tumors will be definitively diagnosed post-operatively.34 35
Phyllodes tumors are classified as benign, borderline, or malignant. Most patients with benign and borderline phyllodes tumors will be cured with surgery, although recurrence rates for all phyllodes lesions are as high as 46%.33 Malignant tumors are very rare. The prognosis is poor if the disease metastasizes, particularly if it metastasizes to the lung.34 35
Emerging evidence suggests that the biology of breast cancer may be influenced by race. This appears to be particularly true for African-American women who have higher mortality rates from breast cancer than white women. Although the difference in survival rates is partially explained through healthcare disparities, such as rates of mammographic screening and access to high quality health care, when these factors are controlled for, the difference remains. One well documented biological difference, for example, is that a significantly higher proportion of black women have breast cancer that is triple-negative (estrogen receptor, progesterone receptor, and HER2 negative) than white women.36
For more information about breast cancer among special populations and for additional information about the clinical presentation, gross pathology, histopathology, clinical course and prognosis of all breast cancers, please refer to Diseases of the Breast (5th edition) by Jay Harris, et al (Eds), 2014. Online sources of additional information can be found on the Additional Resources page.
Types of Breast Cancers
||Typical Clinical Presentation
||Age at Diagnosis
||Hormone Receptor Status
|Ductal Carcinoma In Situ (DCIS)
||Abnormal mammography12 13
||Rare in younger women. Incidence rises rapidly after the age of 40 and peaks at 65-6912
||ER and PR positive in low grade; ER positive in 30-90% of intermediate and high grade: PR variable in intermediate and high grade12
||Negative for low grade; positive for high grade12
||Excellent. Ten year survival rate 96-98%13 14
|Invasive Breast Carcinomas
|Invasive Ductal Carcinoma (IDC)
||Palpable mass and/or abnormal mammography21
||Risk increases with age22
||Positive for ER and/or PR in 70-80% of cases21
||Positive in 15% of cases21
||Varies according to tumor morphology, grade, hormone receptor status, HER2 expression, patterns of gene expression, and the presence of lymphovascular invasion21
|Invasive Lobular Carcinoma (ILC)
||Palpable mass or abnormal mammography. Findings tend to be more subtle than with IDC. Commonly bilateral and multicentric21
||Average age of diagnosis is older than for IDC24
||Typically positive for ER and PR 21 25
||Similar to IDC, perhaps more favorable21
|Other Types of Invasive Breast Cancer
|Inflammatory Breast Cancer (IBC)
||Breast enlargement, warmth, thickening or dimpling of hair follicles (peau d'orange), ridges28
||Mean age of diagnosis is 5828
||More likely to be negative for ER and PR28 29
||Positive in 60% of cases28 29
|Paget's Disease of the Nipple
||Erythema and scaling of nipple skin, nipple tingling, itching, sensitivity, pain, burning or oozing. Half present with palpable mass31
||Mean age of diagnosis is 6230
||Negative for ER and PR in approximately 70% of cases32 33
||Positive in most cases32 33
||Variable depending on the stage underlying tumors. Presence of a palpable mass and spread to lymph nodes associated with a poor prognosis33
||Painless, palpable, rapidly growing mass34
||Mean age of diagnosis is in the 42-4535
||Data limited; hormone receptor status of unknown clinical utility
||Excellent if benign or borderline. If malignant, 10 year survival rate as low as 42%. High incidence of recurrence34
1Collins, L. C., & Schnitt, S. J. (2014). Pathology of benign breast disorders. In J. Harris, M. E. Lippman, M. Morrow, & C. K. Osborne (Eds.), Diseases of the breast, 5th edition (pp 71-88). Philadelphia, PA: Wolters Kluwer Health.
2American Cancer Society. (2014, January 14). Non-cancerous breast conditions. Retrieved from: http://www.cancer.org/Healthy/FindCancerEarly/WomensHealth/Non-CancerousBreastConditions/index
3National Cancer Institute. (2012, November 2). Understanding breast changes: a health guide for women. Retrieved from: http://www.cancer.gov/cancertopics/screening/understanding-breast-changes/understanding-breast-changes.pdf
4Sabel, M. S. (2013, March 6). Overview of benign breast disease. Retrieved from the Up to Date website: http://www.uptodate.com/contents/overview-of-benign-breast-disease
5American Cancer Society. (2014, January 14). How non-cancerous breast conditions affect breast cancer risk. Retrieved from: http://www.cancer.org/healthy/findcancerearly/womenshealth/non-cancerousbreastconditions/non-cancerous-breast-conditions-benign-br-cond-and-br-cancer-risk
6Hartmann, L. C., Sellers, T. A., Frost, M. H., Lingle, W. L., Degnim, A. C., Ghosh, K.,…Visscher, D. W. (2005). Benign breast disease and the risk of breast cancer. (2005). New England Journal of Medicine, 353(3): 229-237. doi:10.1056/NEJMoa044383
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8Degnim, A. C., Visscher, D. W., Berman, H. K., Frost, M. H., Sellers, T. A., Vierkant, R. A…Hartmann, L. C. (2007). Stratification of breast cancer risk in women with atypia: a Mayo cohort study. Journal of Clinical Oncology, 25(19): 2671-2677. doi: 10.1200/JCO.2006.09.0217
9King, T. A, & Reise-Filho, J. S. (2014).Lobular carcinoma in situ: biology and management. In J. Harris, M. E. Lippman, M. Morrow, & C. K. Osborne (Eds.), Diseases of the breast, 5th edition (pp 324-336). Philadelphia, PA: Wolters Kluwer Health.
10Chuba, P. J., Hamre, M. R., Yap, J., Severson, R. K., Lucas, D., Shamsa, F., & Aref, A. (2005). Bilateral risk for subsequent breast cancer after lobular carcinoma-in-situ: Analysis of surveillance, epidemiology, and end results data. Journal of Clinical Oncology, 23(24): 5534-5541. doi: 10.1200/JCO.2005.04.038
11Reis-Filho, J. S., & Pinder, S. E. (2007). Non-operative breast pathology: lobular neoplasia. Journal of Clinical Pathology, 60:1321-1327. doi: 10.1136/jcp.2006.040642
12Corben, A. D., & Brogi, E. (2014). Ductal Carcinoma in situ and other intraductal lesions: Pathology, immunohistochemistry, and molecular alterations. In J. Harris, M. E. Lippman, M. Morrow, & C. K. Osborne (Eds.), Diseases of the breast, 5th edition (pp 309-323). Philadelphia, PA: Wolters Kluwer Health.
13Van Zee, K. J., White, J., Morrow, M., & Harris, J. (2014). Ductal carcinoma in situ and microinvasive carcinoma. In J. Harris, M. E. Lippman, M. Morrow, & C. K. Osborne (Eds.), Diseases of the breast, 5th edition (pp 337-359). Philadelphia, PA: Wolters Kluwer Health.
14Allegra, C. J., Aberle, D. R., Ganschow, P., Hahn, S. M., Lee, C. N., Millon-Underwood, S…Zon, R. (2010). National Institutes of Health State-of-the-Science Conference Statement: Diagnosis and Management of Ductal Carcinoma In Situ September 22-24, 2009. Journal of the National Cancer Institute, 102(3):161-169. doi: 10.1093/jnci/djp485
15Bleiweiss, I. J. (2013, December 19). Pathology of breast cancer. Retrieved from the Up to Date website: http://www.uptodate.com/contents/pathology-of-breast-cancer
16Bane, A. (2013). Ductal carcinoma in situ: What the pathologist needs to know and why. International Journal of Breast Cancer, vol. 2013, Article ID 914053, 7 pages. doi:10.1155/2013/914053.
17The Consensus Conference Committee (1997). Consensus conference on the classification of ductal carcinoma in Situ. Cancer, 80(9): 1798–1802. doi: 10.1002/(SICI)1097-0142(19971101)80:9<1798::AID-CNCR15>3.0.CO;2-0
18College of American Pathologists. (2011, December 13). Definition of synoptic reporting. Retrieved from: http://www.cap.org/apps/docs/committees/cancer/cancer_protocols/synoptic_report_definition_and_examples.pdf
19Howlader, N., Noone, A. M., Krapacho, M., Garshell, J., Neyman, N., Altekruse, S. F…Cronin, K. A. (Eds). SEER Cancer Statistics Review, 1975-2010, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2010/ based on November 2012 SEER data submission, posted to the SEER website, April 2013. Retrieved on Mar 20, 2014 at: http://seer.cancer.gov/csr/1975_2010/sections.html
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21Dillon, D., Guidi, A. J., & Schnitt, S. J.(2014). Pathology of invasive breast cancer. In J. Harris, M. E. Lippman, M. Morrow, & C. K. Osborne (Eds.), Diseases of the breast, 5th edition (pp 381-410). Philadelphia, PA: Wolters Kluwer Health.
22American Cancer Society. (2015, August 19). Breast Cancer. Retrieved from: Invasive ductal carcinoma. Retrieved from: http://www.cancer.org/acs/groups/cid/documents/webcontent/003090-pdf.pdf
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25Lal, P., Tan, L. K., & Chen, B. (2005). Correlation of HER-2 status with estrogen and progesterone receptors and histologic features in 3,655 invasivee breast carcinomas. Am J Clin Pathol, 123: 541-546.
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29Merajver, S. D. (2013, July 25). Inflammatory breast cancer: pathology and molecular pathogenesis. Retrieved from the Up to Date website: http://www.uptodate.com/contents/inflammatory-breast-cancer-pathology-and-molecular-pathogenesis
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34Calhoun, K. E., Allison, K. H., Kim, J. N., Rahbar, H., & Anderson, B. O. (2014). Phyllodes tumors. In J. Harris, M. E. Lippman, M. Morrow, & C. K. Osborne (Eds.), Diseases of the breast, 5th edition (pp 826-837). Philadelphia, PA: Wolters Kluwer Health.
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36Reeder-Hayes, K. E., Wheeler, S. B., & Carey, L. A. (2014). Breast cancer in minority women. In J. Harris, M. E. Lippman, M. Morrow, & C. K. Osborne (Eds.), Diseases of the breast, 5th edition (pp 1112-1124-837). Philadelphia, PA: Wolters Kluwer Health.
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