Breast Cancer




Breast cancer is a major cause of morbidity and mortality across the world. In the United States, each year about 180,000 new cases are diagnosed with more than 40,000 deaths annually ( ). It is a highly heterogeneous disease, both pathologically and clinically. Although age is the single most common risk factor for the development of breast cancer in women (see Fig. 10.13 ), several other important risk factors have also been identified, including a germline mutation ( BRCA1 and BRCA2 ) ( Table 10.1 ), positive family history, prior history of breast cancer, and history of prolonged, uninterrupted menses (early menarche and late first full-term pregnancy) ( Table 10.2 ).




FIGURE 10.25


PAGET’S DISEASE OF THE BREAST.

In this unique clinical entity, one of the main ducts leading to the nipple becomes engorged with neoplastic cells. Clinically, patients present with an eczematous rash that extends to and involves the areola. This rare condition may or may not be associated with an underlying invasive carcinoma.



FIGURE 10.18


INTRADUCTAL CARCINOMA (COMEDO TYPE).

(A) Low- and medium-power ( inset ) microscopic sections show expanded ducts with central necrosis. (B) At high magnification, cellular pleomorphism is also evident. This feature is seen to a greater extent and more commonly in the comedo type of ductal carcinoma in situ. Occult invasive elements may also be more common in the comedo than non-comedo types (see Figs. 10.18 to 10.20 ).



FIGURE 10.13


Age-specific incidence of breast cancer in the United States.


Table 10.1

Estimated Lifetime Incidence of Cancer for BRCA1/2 Mutation Carriers

Adapted from Table 19.1 in .




























Type of Cancer BRCA1 Carrier BRCA2 Carrier
Breast 40–85 40–85
Ovarian 25–65 15–25
Male breast 5–10 5–10
Prostate Elevated * Elevated *
Pancreatic <10 <10

* Prostate cancer risk is probably elevated, but absolute risk is not known.



Table 10.2

Selected Breast Cancer Risk Factors
















































































































Risk Factor Referent Comparison Approximate Relative Risk Selected References
Age (years)
Age at menarche <12 >14 1.2–1.5
Oral contraceptives None Current 1.1–1.2
Age at first birth <20–22 >28–35 1.3–1.8
Breast feeding None 12 months 0.90
Parity 0 5+ 0.6
Age at menopause
Surgical oophorectomy 50+ <40 0.6
Estrogen + progesterone None Current use for 5 years 1.2–1.3
Body mass index
Premenopausal <21 >31 0.5–0.7
Postmenopausal <21 >28–30 1.2–1.3
Physical activity None Moderate 0.60–0.90
Serum estradiol (postmenopausal) Lowest quartile Highest quartile 2
Mammographic breast density <25% density >75% density 4–6
Bone density Lowest quartile Highest quartile 2.0–3.5
Alcohol consumption None 3+ drinks per day 1.3–1.4
Benign breast disease (atypical hyperplasia) No Yes 2–6
Family history of breast cancer in first-degree relative None 1+ 2–4


Much progress has been made in the diagnosis and treatment of primary and metastatic breast cancer. The widespread use of routine mammography has led to an increased incidence in the detection of early primary lesions, a factor that has contributed to a significant decrease in mortality (see Figs. 10.38 to 10.41 , 10.44 ). Magnetic resonance imaging (MRI) of the breast may be useful in screening women with a higher lifetime risk of breast cancer, such as those women with a BRCA1/2 mutation or with a family history strongly suggestive of a hereditary breast/ovarian syndrome ( ) (see Fig. 10.7 ). Moreover, less aggressive, conservative local therapy has been shown to be as effective as mastectomy in prolonging survival, while avoiding the cosmetic disfigurement associated with more extensive surgery. Sentinel node biopsy (see Fig. 10.78 ) is now routinely being offered to appropriate patients, with a significant decrease in the morbidity associated with the traditional axillary node dissection. Adjuvant systemic therapy, such as chemotherapy and/or hormonal therapy, has also contributed to the prolonged survival of patients with breast cancer ( ). The identification of molecular targets such as the overexpression of HER2/neu has allowed biologic therapies directed against the HER2/neu pathway to be considered part of standard treatment in both the adjuvant and metastatic setting for tumors that overexpress HER2/neu ( ).




FIGURE 10.38


LYMPHATIC SPREAD OF BREAST CANCER.

Lymph node metastases are present at the time of diagnosis in up to 60% of cases. In general, lateral lesions in the breast metastasize to axillary and supraclavicular nodes, whereas medial tumors tend to metastasize to the internal mammary and mediastinal lymph nodes, as well as the supraclavicular nodes. However, lymph node involvement is merely a marker for the probability that the cancer has spread from the breast. A positive finding implies that microdeposits of breast cancer will probably be present in other areas as well.



FIGURE 10.39


STAGE I (T1N0) BREAST CANCER.

Magnified view of a screening mammogram from a 52-year-old woman who had no palpable mass demonstrates the classic clustered microcalcifications of several shapes and sizes highly suggestive of carcinoma. Some show linear branching, which is even more suggestive of a ductal lesion. Biopsy confirmed an early invasive ductal carcinoma.

(Courtesy of Dr. P. Stomper, Roswell Park Memorial Institute, Buffalo, NY.)



FIGURE 10.40


STAGE (T1N0) BREAST CANCER.

Magnified view of a mammogram from a 50-year-old woman with a history of “lumpy” breasts shows a 1.0-cm stellate mass in the superior portion of the breast. The lesion was excised and found to be an invasive ductal carcinoma.

(Courtesy of Dr. P. Stomper, Roswell Park Memorial Institute, Buffalo, NY.)



FIGURE 10.41


STAGE IIA (T2N0) BREAST CANCER.

This mammogram from a 65-year-old woman shows that the breasts are not too dense; therefore, the 2.5-cm stellate mass in the upper outer quadrant of the right breast was easily palpated. Histologic examination following resection showed an invasive ductal carcinoma.



FIGURE 10.44


STAGE IIB (T4) BREAST CANCER.

Classically, inflammatory breast cancer does not present as a discrete mass but instead as cutaneous erythema with overlying skin warmth, as illustrated in the left breast of this 63-year-old patient.



FIGURE 10.7


(A) Bilateral mammograms on a 45-year-old patient with enlarged right axillary nodes ( black arrow ) but no mammographic abnormality within either breast. (B) Sagittal MR image of the right breast with fat saturation before administration of gadolinium. A rounded density represents an axillary node ( white arrow ). (C) Sagittal MR image at the same location as B after administration of gadolinium. Enhancement of the node is evident ( white arrow ). (D) Sagittal MR image of the right breast at a level slightly medial to B and C . A patch of stromal density is evident deep in the breast before contrast administration ( white arrow ). Other retroareolar stromal densities with similar appearance are also present. (E) Sagittal MR image of the right breast in the same location as D , after administration of gadolinium. The deep stroma is enhancing ( white arrow ) consistent with tumor, while the other stromal densities have not changed, consistent with normal breast tissue.



FIGURE 10.80


COMPLICATIONS OF CHEMOTHERAPY.

Chemotherapy can also produce integumentary toxicity. This patient had metastatic breast cancer and was treated with high-dose doxorubicin. After her first course she noticed a change in her fingernails. She went on to develop onycholysis and onychomadesis. Although uncommon, this is a potential complication of doxorubicin.


Incidence


Breast cancer incidence has remained level during the last decade. Breast cancer deaths are decreasing, primarily for white women and younger women. Although white women develop breast cancer more frequently, black women are more likely to die of the disease ( ) ( Fig. 10.8A, B ).




FIGURE 10.8


(A) Five-year relative survival by race and stage at diagnosis of breast cancer (SEER data, 1996–2002). (B) Female breast cancer incidence by race and ethnicity (SEER data). (C) When lobular breast cancer metastasizes it can often infiltrate serosal surfaces mimicking ovarian cancer. This patient presented with abdominal bloating, tightness, and narrowing in her stool caliber 9 years after the diagnosis of a stage I breast cancer. Note the diffuse thickening of the rectal and colonic wall, peritoneal carcinomatosis, and ascites. A colonoscopy was performed, and biopsy confirmed diffuse involvement with metastatic adenocarcinoma consistent with a breast primary. On restaging, she was also noted to have multiple osseous metastases. (Image courtesy of Drs. Pamela Dipiro and Wendy Chen, Dana Farber Cancer Institute, Boston, MA.) (D) In an ultrasound-guided needle biopsy, the ultrasound probe is used to localize the lesion that was identified either on physical examination or on mammogram. A biopsy needle is passed through the lesion several times to obtain tissue. Compared to a stereotactic biopsy, an ultrasound-guided biopsy is faster and better tolerated by most patients. However, not all lesions may be amenable to an ultrasound-guided biopsy. (Image courtesy of Robyn L. Birdwell, MD, Brigham and Women’s Hospital, Boston, MA, and Diagnostic Imaging Breast, Amirsys, Inc., Salt Lake City, UT, 2006.) (E) The premise behind stereotactic needle biopsy is that a lesion can be localized in three dimensions by evaluating its changes in position in a series of angled radiographic views. First, a radiograph localizes the suspicious area, then two additional views, angled 15 degrees to either side of the lesion, are obtained. A computer calculates how much the lesion’s position appears to have changed on each of the angled views and uses these data to estimate the lesion’s location within three-dimensional space. With the advent of digital mammography these images are commonly acquired digitally. (Image courtesy of Robyn L. Birdwell, MD, Brigham and Women’s Hospital, Boston, MA, and Diagnostic Imaging Breast, Amirsys, Inc., Salt Lake City, UT, 2006). (F) Positron emission tomography (PET) involves injection of a substance labeled with a positron-emitting isotope (commonly, fluorine-18 bound to d -glucose, called FDG for 2-([ 18 F]fluoro-2-deoxy- d -glucose)). Metabolically active cells, especially malignant ones, preferentially take up glucose, and therefore FDG, as compared with non-neoplastic tissue. Sensitivity of PET can vary considerably by tumor type and size. False-positive results can occur in areas of inflammation or infection. Many machines now acquire CT images in tandem with PET images, which can then be fused together to provide anatomic correlation by CT with metabolic activity measurements by PET. This patient presented with palpable axillary adenopathy and a large breast mass with associated erythema, skin edema, and nipple retraction. Note the extremely intense areas of uptake within the right breast and axilla corresponding to the patient’s known locally advanced breast cancer. Also note the intense uptake in the right supraclavicular, paratracheal, prevascular, precarinal, and hilar lymph nodes suspicious for metastatic disease. Uptake in the kidney, bladder, and ureters is physiologic and due to FDG excretion. Uptake in the right adnexa and jaw is most likely physiologic and benign. (G) Panels 1 and 2: Accelerated partial breast irradiation (APBI) encompasses techniques including intracavitary and interstitial brachytherapy as well as 3D-conformal, intensity-modulated, and intraoperative external-beam radiation therapy. One of the more commonly used brachytherapy methods in the United States, the MammoSite Brachytherapy System (Hologic, Massachusetts) involves insertion of a catheter with a balloon tip into the lumpectomy cavity at the time of surgery or shortly thereafter (panel 1). The balloon is filled with saline and a high-dose-rate radioactive source is introduced twice per day for 5 days by computed axial tomography scan–based treatment planning, permitting a highly conformal dose to be delivered to the first centimeter of remaining breast tissue with optimal sparing of the remaining tissue and other regional organs (panel 2). The balloon catheter is removed upon completion. APBI is an option only for selected patients, mainly older women with smaller, node-negative “low-risk” tumors and with negative margins. (Courtesy of Phillip M. Devlin, MD, Dana Farber/Brigham and Women’s Cancer Center, Harvard Medical School, Boston, MA.) (H) The HER family of receptors (human epidermal growth factor receptor, also called ErbB) is a group of transmembrane tyrosine kinase receptors that regulate cell growth, survival, and differentiation, via a variety of pathways, including RAS (rat sarcoma), RAF (receptor activation factor), MAPK (mitogen-activated protein kinase), and MEK (mitogen extracellular signal kinase). The tyrosine kinase domains are activated by dimerization. Current therapeutics involve tyrosine kinase inhibitors (e.g., lapatinib) and antibodies directed against the HER2 protein and VEGF (vascular endothelial growth factor)(e.g., trastuzumab and bevacizumab).




Screening


Routine mammographic screening allows better detection of primary breast cancers than physical examination. Mammographic screening has been shown to decrease mortality rates in women 50–69 years of age. A 26% decrease in the relative risk of breast cancer was noted with screening mammography in this group. The role of screening mammography in women 40–49 years of age also appears to be associated with a reduction in breast cancer mortality, but of slightly smaller magnitude ( ). Current imaging modalities include mammography, ultrasound, and, recently, MRI. Only mammography has been demonstrated to be a valuable tool in decreasing mortality.


Over half of all women will develop benign breast lesions. These include macro- and microcysts, adenosis, apocrine changes, intraductal papillomas, fibrosis, fibroadenomas, and epithelial hyperplasias (see Figs. 10.2 to 10.6 and 10.9 to 10.12 ). Only the latter, however, particularly those showing atypia, are believed to be precursors to the development of malignancy ( ). Benign lesions may present with pain, tenderness, and nipple discharge, as well as masses and dimpling of the skin. Mammographic changes, such as densities and microcalcifications, may also be noted in benign lesions and at times, may mimic malignancies.




FIGURE 10.2


FIBROADENOMA.

The tumor from which this histologic section was taken was a well-circumscribed, discoid mass, clearly demarcated from the surrounding breast tissue. High magnification reveals stroma compressing ducts so that they form slitlike curvilinear spaces. Note the low cellularity of the stroma, an important benign feature.



FIGURE 10.3


LACTATING ADENOMA.

This well-circumscribed lesion has closely packed acini with prominent epithelial cells marked by large nuclei and abundant, pink, vacuolated cytoplasm.

(Courtesy of Dr N. Weidner, Brigham and Women’s Hospital, Boston, MA.)



FIGURE 10.4


SCLEROSING ADENOSIS.

(A) Low-power microscopic section shows distortion of the lobular architecture; there is an increase in acini (terminal ductules), appearing in a whorled, expansile, and vaguely defined pattern. The low-power view is very helpful in distinguishing this benign proliferation from malignancy. (B) Higher magnification shows that the acini are composed of a normal two-cell population.



FIGURE 10.5


PAPILLOMA.

Low-magnification view shows a large duct filled with a papillary proliferation. At higher power ( inset ) a papillary branch can be seen with a normal two-cell population covering a fibrovascular stalk. In this benign tumor the lining epithelial cells can show apocrine changes.



FIGURE 10.6


FIBROCYSTIC CHANGES.

These benign changes are the most common findings in breast biopsies. They are characterized by dense fibrosis intermixed with cystic areas.



FIGURE 10.9


EPITHELIAL HYPERPLASIA (MILD).

This lobular unit shows irregular areas of heaped-up cells lining the acini (terminal ductules). At high magnification ( inset ) the epithelial layer of one ductule is three to four cell layers thick, and there is no bridging of cells across the acinar structure.



FIGURE 10.10


EPITHELIAL HYPERPLASIA (MODERATE).

At this stage the acinar structure is distended by hyperplastic cells that frequently bridge the lumen, often filling as much as half of it.



FIGURE 10.11


EPITHELIAL HYPERPLASIA (FLORID).

Involved spaces show marked distention by hyperplastic cells that occupy the majority of the lumen. Collapsed slitlike spaces are present, frequently at the periphery of the structure. These slits are surrounded by serpentine passages composed of “flowing” cells, which often lack clear cell borders. Moderate and florid hyperplasias imply a slightly higher risk of subsequent invasive carcinoma than mild or no hyperplasia.



FIGURE 10.12


EPITHELIAL HYPERPLASIA (ATYPICAL).

(A) Atypical cases show a nonuniform population of cells from normochromatic nuclei surrounding spaces that are not quite smooth-lined. It is these features that distinguish atypical epithelial (ductal) hyperplasia from ductal carcinoma in situ, in which smooth, geometric spaces are surrounded by a uniform cell population with hyperchromatic nuclei. (B) High magnification shows that these proliferating, relatively nonuniform cells lack the necessary degree of cell-to-cell rigidity. Atypical hyperplasia carries a relatively higher risk of subsequent development of invasive carcinoma than other types. This risk is further elevated in women with a family history of breast cancer in a first-degree relative.




Histology


IN SITU BREAST CANCERS AND NONINVASIVE BREAST CANCER


The enthusiasm for screening has led to the detection of small primary lesions that pose difficult diagnostic dilemmas when breast biopsies reveal premalignant histopathologic findings. The diagnosis of in situ carcinomas appears to be increasing in frequency. Noninvasive breast cancer includes ductal carcinoma in situ (DCIS) and lobular carcinoma in situ (LCIS). DCIS is described as the proliferation of malignant epithelial cells confined to the mammary ducts without evidence of invasion through the basement membrane (see Figs. 10.14 , 10.16 to 10.20 , and 10.22 ) and is considered a precursor lesion. DCIS (also called intraductal carcinoma) is more likely to be localized to a region within one breast. Variants include papillary carcinoma in situ (see Fig. 10.21 ) which may mimic benign atypical papillomatosis, and comedo carcinoma, which consists of a solid growth of neoplastic cells within the ducts, associated with centrally located necrotic debris ( ).




FIGURE 10.14


Timeline of breast cancer suggesting probable heterogeneity. Primary breast cancers begin as single (or more) cells that have lost normal regulation of differentiation and proliferation but remain confined within the basement membrane of the duct or lobule. As these cells go through several doublings, at some point they invade through the basement membrane of the ductule or lobule and ultimately metastasize to distant organs.



FIGURE 10.16


SYSTEMIC THEORY OF BREAST CANCER SPREAD.

This theory suggests that breast cancer becomes metastatic very early in its course, once invasion through the basement membrane of the duct or lobule has occurred. It maintains that local therapy will have few if any long-term effects on survival, because the disease is already systemic at the time of diagnosis.



FIGURE 10.17


INTRADUCTAL CARCINOMA (CRIBRIFORM TYPE).

(A) Low- and (B) high-power photomicrographs demonstrate a cribriform pattern composed of a rather uniform tumor cell population with distinct cytoplasmic borders; the cells are rigidly arranged around crisp, circular holes. With this pattern the risk for the subsequent development of invasive cancer increases 10- to 11-fold.

(Courtesy of Dr N. Weidner, Brigham and Women’s Hospital, Boston, MA.)



FIGURE 10.19


INTRADUCTAL CARCINOMA (“CLINGING” TYPE).

Low- (inset) and high-power microscopic sections show tumor cells “clinging” to the periphery of a duct. The clusters of basophilic malignant cells show a high nucleus-to-cytoplasm ratio. Note the bridgelike structure formed by these cells on the high-power view.



FIGURE 10.20


INTRADUCTAL CARCINOMA (MICROPAPILLARY TYPE).

(A) Low magnification reveals expanded ducts with fronds of tumor characteristically extending toward the center of the lumina. (B) At high magnification the bulbous fronds typically appear narrow at the base and expanded at the tip.

( A , Courtesy of Dr N. Weidner, Brigham and Women’s Hospital, Boston, MA.)



FIGURE 10.22


INTRADUCTAL CARCINOMA.

(A) Microscopic section shows a normal lobular unit on the left and “cancerization of the lobules” on the right, where a ductal carcinoma has extended into the lobules. (B) High magnification demonstrates “cancerization of the lobules” in the upper portion of the field, whereas the lower portion reveals a duct that has been expanded by an intraductal carcinoma with foci of necrosis. “Cancerization of the lobules” carries no clinical significance except that it may mimic lobular carcinoma in situ. However, pleomorphism, tubule formation, and necrosis, as seen here, are not encountered in lobular carcinoma.



FIGURE 10.21


PAPILLARY CARCINOMA IN SITU.

The architectural features of this in situ breast cancer are similar to those of a papilloma. The normal two-cell–layer epithelium covering the fibrovascular fronds is replaced by a uniform proliferation of cells with hyperchromatic nuclei.


In contrast, LCIS (see Figs. 10.23 , 10.24 ) tends to be diffusely distributed throughout both breasts. LCIS is considered a risk factor for breast cancer and is not a precursor lesion ( ).




FIGURE 10.23


LOBULAR CARCINOMA IN SITU.

Low-power photomicrographs show (A) the normal architecture of a lobular unit and (B) a distended lobular unit showing the typical appearance of LCIS. (C) At high magnification the lobular unit is seen to be distended and distorted by characteristically uniform, round tumor cells with bland nuclei. LCIS is usually diffusely dispersed throughout the breast and is often bilateral. Rarely producing a mass or abnormality on mammography, it is commonly discovered coincidentally during a biopsy performed for other suspicious lesions. Women with LCIS have a slightly higher risk of developing invasive cancer, whether ductal or lobular in origin, in their lifetime.



FIGURE 10.24


LOBULAR CARCINOMA IN SITU.

High-power microscopic section shows clusters of tumor cells spreading along a duct in a “pagetoid” fashion; that is, displacing the normal ductal epithelium toward the lumen, which is lined by attenuated luminal surface cells. This should not be confused with Paget’s disease of the breast, a lesion of ductal origin, in which tumor cells extend into the epidermis (see Fig. 10.25 ).


DCIS is more common than LCIS, representing about 20% of breast cancers diagnosed in the United States ( ). Although the prognosis for patients with both types of in situ lesions is excellent, invasive lesions will develop in a certain fraction of patients with in situ carcinomas. Surgery, as either mastectomy or breast-conserving surgery plus adjuvant radiation, has been the treatment of choice for DCIS ( ). Selective estrogen receptor modulators, such as tamoxifen, may further decrease recurrence risk ( ). Management options for LCIS include careful observation or bilateral prophylactic simple mastectomy or the use of tamoxifen.


INVASIVE BREAST CANCERS


Over 75% of all infiltrating breast cancers originate in the ductal system (see Figs. 10.1 , 10.27 to 10.29 ; Table 10.3 ). Several histologic variants of ductal carcinoma have been described. Pure examples of these variants constitute only a small percentage of the total number of cases, but certain features of each may be seen within the main portions of tumors that show the more common presentation designated invasive (or infiltrating) ductal carcinoma. Medullary carcinoma (see Fig. 10.32 ) is distinguished by poorly differentiated nuclei and infiltration by lymphocytes and plasma cells, whereas tubular carcinomas (see Fig. 10.31 ) are highly differentiated tumors that are marked, as their name suggests, by tubule formation. In mucinous (or colloid) carcinomas (see Fig. 10.33 ), nests of neoplastic epithelial cells are surrounded by a mucinous matrix. A few invasive ductal carcinomas exhibit papillary features; hence their designation as papillary carcinomas. Although the above variants may carry a more favorable prognosis than routine infiltrating ductal carcinomas, they are treated similarly, based on stage of disease.




FIGURE 10.1


BREAST ANATOMY.

Within the breast the epithelial elements are organized into lobular units consisting of acini that feed into ductules. The latter in turn coalesce into larger ducts that form a reservoir, or lactiferous sinus, proximal to the nipple. These epithelial structures, supported by adipose and fibrous tissue, give rise to more than 95% of breast malignancies.



FIGURE 10.27


INVASIVE DUCTAL CARCINOMA.

Low- and high-power ( inset ) photomicrographs of a poorly differentiated adenocarcinoma show that the stroma is infiltrated by pleomorphic tumor cells showing a high mitotic rate. Note the necrosis and lack of tubule formation.



FIGURE 10.28


INVASIVE DUCTAL CARCINOMA.

Low magnification of a breast biopsy specimen stained for estrogen receptor protein (ERP) using an estrogen receptor immunocytochemical assay (ERICA) shows that most cells are positive ( brown ). ERICA allows for semiquantitation of ERP. High magnification ( inset ) reveals that the antibody is localized to the nuclei ( brown ).

(Courtesy of Dr. S.L. Khoury, Brigham and Women’s Hospital, Boston, MA.)



FIGURE 10.29


INVASIVE DUCTAL CARCINOMA.

Photomicroscopic section of a breast biopsy specimen demonstrates an invasive ductal carcinoma in the lymphatic vessels of the breast parenchyma.


Table 10.3

Incidence of Histologic Types of Invasive Breast Cancer from SEER *

From .


































Type Frequency (%)
Ductal 75.8
Lobular 8.3
Ductolobular 7.1
Mucinous (colloid) 2.4
Comedocarcinoma 1.6
Inflammatory 1.6
Tubular 1.5
Medullary 1.2
Papillary <1

* Note: Other miscellaneous tumors (e.g., metaplastic, adenocystic, micropapillary, apocrine, Paget’s) were not included in the above list. They compose <5% of invasive breast cancers.




FIGURE 10.32


MEDULLARY CARCINOMA.

(A) Low-power photomicrograph of this histologic variant of invasive ductal carcinoma demonstrates its characteristic syncytial growth pattern. The tumor has a smooth, well-circumscribed border and shows a prominent lymphocytic infiltrate. (B) At higher magnification, the classic pleomorphic cells with bizarre nuclei are evident. This malignancy has better 5- and 10-year survival rates than common ductal carcinoma.

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Aug 13, 2019 | Posted by in ONCOLOGY | Comments Off on Breast Cancer

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