(Radiographics. 1999;19:245-247.)
© RSNA, 1999
Breast Imaging Case of the Day
Dvora Cyrlak, MD1,
Philip M. Carpenter, MD2 and
Niraj B. Rawal, BS3
1 Departments of Radiological Sciences (D.C.)
2 Pathology (P.M.C.)
3 University of California, Irvine Medical Center (N.B.R.), 101 The City Drive, Orange, CA 92868-3298.
Index Terms: Breast neoplasms, calcification, 01.815 • Breast neoplasms, diagnosis • Breast neoplasms, radiography, 01.11
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HISTORY
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A 63-year-old asymptomatic woman who had undergone right mastectomy for breast carcinoma 11 years earlier presented for screening mammography of the left breast.
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FINDINGS
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Standard craniocaudal and mediolateral oblique mammograms demonstrated a 1.5-cm multilobulated, spiculated mass in the left upper outer quadrant (Fig 1a, 1b). Magnification view in the mediolateral projection also demonstrated fine, punctate microcalcifications associated with the mass (Fig 1c). Stereotactically guided core needle biopsy was performed initially, and mammographic needle localization with open surgical biopsy was performed later.
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Figure 1a. (a, b) Craniocaudal (a) and mediolateral oblique (b) mammograms of the left breast demonstrate a 1.5-cm multilobulated, spiculated mass in the upper outer quadrant. (c) Coned compression magnification view in the mediolateral projection also demonstrates faint punctate microcalcifications. The original mammograms (not shown) demonstrated approximately 10 microcalcifications.
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Figure 1b. (a, b) Craniocaudal (a) and mediolateral oblique (b) mammograms of the left breast demonstrate a 1.5-cm multilobulated, spiculated mass in the upper outer quadrant. (c) Coned compression magnification view in the mediolateral projection also demonstrates faint punctate microcalcifications. The original mammograms (not shown) demonstrated approximately 10 microcalcifications.
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Figure 1c. (a, b) Craniocaudal (a) and mediolateral oblique (b) mammograms of the left breast demonstrate a 1.5-cm multilobulated, spiculated mass in the upper outer quadrant. (c) Coned compression magnification view in the mediolateral projection also demonstrates faint punctate microcalcifications. The original mammograms (not shown) demonstrated approximately 10 microcalcifications.
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DIAGNOSIS: Florid sclerosing adenosis.
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DISCUSSION
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Sclerosing adenosis occurs as part of a spectrum of proliferative abnormalities referred to as fibrocystic changes (1). Although sclerosing adenosis may manifest as a clinically palpable mass (adenosis tumor), it is more commonly detected only at mammography.
Sclerosing adenosis may be focal or diffuse at mammography; that is, it may appear as a focal cluster of microcalcifications or as diffuse calcifications. A focus of sclerosing adenosis may be associated with a nodule or with a spiculated lesion, as in this case (1–3).
As the name implies, sclerosing adenosis is a combination of stromal sclerosis and proliferative adenosis pathologically (Fig 2a). Adenosis manifests as a lobulocentric lesion that is largely derived from the terminal ductal lobular unit (TDLU) (1). This condition involves proliferation of ductules and lobules in the TDLU. Both epithelial and myoepithelial cells proliferate. In florid adenosis, hyperplasia of epithelial and myoepithelial cells is associated with distortion and effacement of the underlying lobules. Nuclear pleomorphism and an increase in cell size occur, and the TDLU enlarges (1). In sclerosing adenosis, there is stromal sclerosis involving half or more of the TDLU (4), which is elongated, distorted, and compressed by the sclerosis. Myoepithelial proliferation is a prominent finding (Fig 2b). Sclerosing adenosis contains calcifications in about 50% of cases (5). Calcifications are more common and extensive in sclerosing adenosis than in florid adenosis (1).
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Figure 2a. (a) Low-power photomicrograph (original magnification, x40; hematoxylin-eosin stain) shows glandular structures of varying sizes (adenosis) with the smaller glands compressed by surrounding stromal sclerosis. (b) Low-power photomicrograph (original magnification, x40; immunoperoxidase stain with monoclonal antibody HHF-35) demonstrates a layer of cells immunoreactive for muscle actin around each of the small glands. The presence of these myoepithelial cells suggests a benign process (adenocarcinoma of the breast usually has no myoepithelium).
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Figure 2b. (a) Low-power photomicrograph (original magnification, x40; hematoxylin-eosin stain) shows glandular structures of varying sizes (adenosis) with the smaller glands compressed by surrounding stromal sclerosis. (b) Low-power photomicrograph (original magnification, x40; immunoperoxidase stain with monoclonal antibody HHF-35) demonstrates a layer of cells immunoreactive for muscle actin around each of the small glands. The presence of these myoepithelial cells suggests a benign process (adenocarcinoma of the breast usually has no myoepithelium).
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Sclerosing adenosis may present a diagnostic dilemma for the pathologist because stromal sclerosis and elastosis may mimic infiltrating carcinoma (3). Tubular carcinoma in particular presents a difficulty in differential diagnosis. Absence of the basement membrane and of myoepithelial cells in tubular carcinoma (and their presence in sclerosing adenosis) is helpful in differentiation (5,6). The pathologist must also differentiate sclerosing adenosis from radial scar, which is characterized by more extensive sclerosis with a central fibrocollagenous scar (5).
At mammography, sclerosing adenosis forms part of a differential diagnosis for spiculated lesions that includes both malignant lesions (eg, infiltrating ductal carcinoma, infiltrating lobular carcinoma, tubular carcinoma, ductal carcinoma in situ) and benign lesions (eg, postoperative scar, radial scar, fat necrosis, tuberculosis) (3).
The mammographic differentiation of benign from malignant spiculated lesions is not reliable. Infiltrating carcinoma tends to have a denser center than either sclerosing adenosis or radial scar (3). Microcalcifications are often present in association with spiculated breast carcinomas but may also occur in benign lesions, including sclerosing adenosis (as in this case), radial scar, and fat necrosis.
Histologic features that are useful for the pathologist usually do not aid in mammographic differential diagnosis of spiculated lesions. With the exception of cases involving clear-cut postoperative scarring or fat necrosis (wherein mammographic-clinical correlation may be sufficient), biopsy is mandatory.
Carcinoma in situ rarely develops in an area of sclerosing adenosis but may mimic invasive carcinoma at pathologic examination (7). The presence of an intact basement membrane and myoepithelial cells, both of which are absent in invasive cancer, aids in differential diagnosis (7). In addition, the underlying architecture of adenosis is not altered when ductal or lobular carcinoma in situ develops. Lobular carcinoma in situ is found more often than ductal carcinoma in situ in areas of sclerosing adenosis (1).
Several studies have addressed whether sclerosing adenosis is a precursor lesion or a risk factor for carcinoma. In 1945, Foote and Stewart (8) studied the frequency of fibrocystic changes in patients with and without breast carcinoma and concluded that adenosis, especially sclerosing adenosis, is neither a precursor nor a risk factor. However, subsequent authors have reported an overall relative risk ranging from 1.7 to 2.5 (4,9,10). In and of itself, sclerosing adenosis appears to cause only a mild increase in the risk of infiltrating breast cancer. When atypical hyperplasia is also present, the relative risk rises markedly to as much as 6.7 (4).
In this case, results of both stereotactically guided core needle biopsy and mammographic needle localization with open surgical biopsy confirmed florid sclerosing adenosis. The patient was followed up for 3 years and is presently doing well.
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Footnotes
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Address reprint requests to D.C.
From the 1998 RSNA scientific assembly.
Received for publication August 7, 1998.
Revision received August 21, 1998. September 10, 1998.
Accepted for publication September 10, 1998.
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References
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Flotte TJ, Bell DA, Greco MA. Tubular carcinoma and sclerosing adenosis: the use of basal lamina as a differential feature. Am J Surg Pathol 1980; 4:75-77.[Medline]
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Foote FW, Jr, Stewart FW. Comparative studies of cancerous versus non-cancerous breast. Ann Surg 1945; 12:6-53.
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Krieger N, Hiatt RA. Risk of breast cancer after benign breast diseases: variation by histologic type, degree of atypia, age at biopsy, and length of follow-up. Am J Epidemiol 1992; 136:619-631.
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Dupont WD, Page DL. Risk factors for breast cancer in women with proliferative breast disease. N Engl J Med 1985; 312:146-151.[Abstract]
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HISTORY
FINDINGS
