Published online before print October 30, 2001, 10.1148/radiol.2213000890
(Radiology. 2001;221:770-773.)
© RSNA, 2001
Case 41: Ductal Carcinoma in Situ1
Alanna T. Harris, MD
1 From the Aventura Breast Diagnostic Center, Aventura Hospital and Medical Center, 20950 NE 27th Ct, Aventura, FL 33180. Received May 2, 2000; revision requested June 13; revision received July 17; accepted July 25. Address correspondence to the author (e-mail: eharris@pol.net).
Index terms: Breast neoplasms, 00.32, 00.3241 Breast neoplasms, calcification, 00.812, 00.813, 00.816 Diagnosis Please
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HISTORY
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A 72-year-old woman presented for her annual screening mammogram. Mammographic results obtained 4 years earlier were negative. The patient had no current breast symptoms and no history of breast disease; she said that she had not undergone previous breast biopsy, aspiration, or galactography and that she had not experienced breast trauma. She had no known family history of breast cancer and had never received hormone replacement therapy. There were no palpable breast abnormalities at physical examination, and there was no evidence of nipple retraction, nipple discharge, or skin thickening. Her medical history included carcinoma of the left lung treated with pneumonectomy 10 years earlier. She also had a history of diabetes, hypothyroidism, hypertension, emphysema, and arthritis.
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IMAGING FINDINGS
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The initial screening craniocaudal (Fig 1) and mediolateral oblique (Fig 2) mammograms of the left breast revealed a branching tubular opacity with peripheral coarse calcifications in the lower inner quadrant. Incidental vascular calcifications and oil cysts were also noted. The spot magnification image (Fig 3) showed in greater detail the branching pattern of the tubular opacity and the pleomorphic characteristics of the peripheral calcifications. Focal ultrasonography (US) (Fig 4) of the left lower inner quadrant revealed only a few minimally dilated ducts. Stereotactic core biopsy was performed, followed by surgical excision, and pathologic findings were consistent with high-grade comedo-type ductal carcinoma in situ (Fig 5).

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Figure 1. Craniocaudal mammogram of the left breast demonstrates a branching tubular opacity (solid straight arrow) in the inner part of the breast. Benign-appearing vascular calcifications (open arrow) and oil cysts (curved arrows) are noted.
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Figure 2. Mediolateral oblique mammogram of the left breast reveals the same branching tubular opacity (solid straight arrow) in the lower portion of the breast. Vascular calcifications (open arrow) and oil cysts (curved arrows) are also seen.
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Figure 5. Photomicrograph shows a cross-section of ducts from the mastectomy specimen. Tumor cells (straight arrows) of intraductal carcinoma and extensive central necrosis containing areas of calcification (curved arrows) are seen. (Hematoxylin-eosin; original magnification, x100.)
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DISCUSSION
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The differential diagnosis of this branching tubular opacity with calcifications includes vascular structures, papillomatosis, contrast material injection, fat necrosis, secretory disease, atypical ductal hyperplasia, and ductal carcinoma in situ. A vascular cause would be unlikely because vessels are usually serpentine. Vascular calcifications typically have a train-track appearance on one or both sides of the vessel that is most opaque at the margins; the calcifications may be inhomogeneous when viewed en face, but they do not produce homogeneously opaque tubular structures as seen in this case (1). Mondor disease, thrombophlebitis of the superficial veins of the breast that can occasionally produce a calcified dilated structure, can be excluded due to the lack of pain, the absence of a palpable cord, and the imaging findings that suggest a ductal rather than a vascular lesion (2).
Papillomatosis, in which multiple papillomas form in peripheral ducts, is not likely because calcifications are usually punctate rather than linear, and associated opacities are typically more masslike and nodular (3). Although the branching tubular opacity resembles a duct opacified during galactography, this possibility is excluded since the patient had not undergone prior ductography, nor would this diagnosis account for the calcifications.
Calcifications of fat necrosis, although typically lucent-centered, can sometimes appear somewhat unusual, but they would not opacify a duct and are also excluded because of the patients lack of a history of previous breast surgery or trauma (1). Secretory calcifications are typically large and rodlike, are occasionally lucent-centered, and are usually bilateral (1). The imaging findings of focal and unilateral fragmented linear and pleomorphic calcifications in this case help to exclude this diagnosis.
Atypical ductal hyperplasia is a proliferative lesion that shares some pathologic features with low-grade ductal carcinoma in situ. However, the calcifications seen with atypical ductal hyperplasia are not associated with central necrosis and are usually clustered, round, punctate, or amorphous rather than linear and branching, as shown in this case (4,5).
The correct diagnosis can be made by carefully analyzing the two major abnormalities on the images. The first finding is the branching tubular opacity, which represents a solitary dilated duct that is distended and opacified by disease. The second abnormality is the concentration of pleomorphic linear ductal calcifications, which represent calcified necrotic debris. Ductal carcinoma in situ, which commonly causes calcifications and occasionally ductal dilatation, is the most likely diagnosis and was confirmed with both stereotactic core biopsy and surgical excision. Histologic correlation of the subsequent mastectomy specimen revealed that the ducts were filled with comedo-type necrotic material that was undergoing microscopically visible calcification, accounting for the opacification of the ducts at mammography (Fig 5).
The detection of ductal carcinoma in situ has increased markedly in recent years secondary to the widespread use of screening mammography, and it now accounts for 25%40% of mammographically detected breast cancers (6,7). Although most patients are asymptomatic, some present with nipple-related disease (nipple discharge or Paget disease) or have palpable abnormalities. Risk factors for ductal carcinoma in situ are similar to those for invasive carcinoma and include increasing age, a family history of breast cancer, nulliparity, and age of 30 years or older at the birth of the first child (8).
There are varied mammographic manifestations of ductal carcinoma in situ, with calcifications being the most common (911). In a study of 100 cases of asymptomatic patients with ductal carcinoma in situ, 72% of the malignancies manifested as microcalcifications, 10% as a soft-tissue opacity, and 12% as both (11). Although ductal carcinoma in situ calcifications may assume varied appearances, linear calcifications are more likely to be associated with comedo-type ductal carcinoma in situ while granular calcifications are more often correlated with noncomedo ductal carcinoma in situ (12).
There are numerous atypical mammographic appearances of ductal carcinoma in situ, including developing opacities, subareolar masses, architectural distortions, rounded tumors, asymmetries, and dilated retroareolar ducts (9). The single dilated duct is considered an indirect sign of malignancy but is more often related to a benign cause. However, when a single dilated duct is associated with malignant-appearing calcifications, as in this case, or if it is palpable, biopsy should be suggested (13,14).
There are several classifications of ductal carcinoma in situ (15,16). Histologic subtypes include the following: high-grade ductal carcinoma in situ, which is characterized by comedo-type necrosis, nuclear pleomorphism, and abundant mitotic figures; low-grade ductal carcinoma in situ, which demonstrates monomorphic nuclei, few mitotic figures, and, rarely, necrosis; and intermediate-grade ductal carcinoma in situ, which occurs in the spectrum between the two (17,18). With the Van Nuys Prognostic Index, tumor size, margin width, and pathologic classification (nuclear grade and necrosis) can be used to predict local recurrence (16).
Treatment options for ductal carcinoma in situ include mastectomy, lumpectomy with breast irradiation, or, for patients with small lesions (<12 cm) of low-grade ductal carcinoma in situ, lumpectomy alone (1921). Because of the pathologic grade and extent of disease in this case, the patient was treated with mastectomy.
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ACKNOWLEDGMENTS
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The author thanks Patricia Parker, MD, Aventura Hospital, Aventura, Fla, for her assistance with the pathologic correlation.
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FOOTNOTES
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Part 1 of this case appeared 4 months previously and may contain larger images.
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REFERENCES
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Cardenosa G, Eklund GW. Benign papillary neoplasms of the breast: mammographic findings. Radiology 1991; 181:751-755.
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Helvie MA, Hessler C, Frank TS, Ikeda DM. Atypical hyperplasia of the breast: mammographic appearance and histologic correlation. Radiology 1991; 179:759-764.
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Cardenosa G. Selected breast lesions: imaging-pathology correlation. In: Dempsey PJ, Monsees B, eds. Breast imaging categorical course syllabus. Leesburg, Va: American Roentgen Ray Society, 1999; 65-66.
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Ernster VL, Barclay J, Kerlikowske K, Grady D, Henderson C. Incidence of and treatment for ductal carcinoma in situ of the breast. JAMA 1996; 275:913-918.
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Sickles EA. Breast imaging: from 1965 to the present. Radiology 2000; 215:1-16.
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Kerlikowske K, Barclay J, Grady D, Sickles EA, Ernster V. Comparison of risk factors for ductal carcinoma in situ and invasive breast cancer. J Natl Cancer Inst 1997; 89:77-82.
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Ikeda DM, Andersson I. Ductal carcinoma in situ: atypical mammographic appearances. Radiology 1989; 172:661-666.
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Dershaw DD, Abramson A, Kinne DW. Ductal carcinoma in situ: mammographic findings and clinical implications. Radiology 1989; 170:411-415.
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Stomper PC, Connolly JL, Meyer JE, Harris JR. Clinically occult ductal carcinoma in situ detected with mammography: analysis of 100 cases with radiologic-pathologic correlation. Radiology 1989; 172:235-241.
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Stomper PC, Connolly JL. Ductal carcinoma in situ of the breast: correlation between mammographic calcification and tumor subtype. AJR Am J Roentgenol 1992; 159:483-485.
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Sickles EA. Mammographic features of 300 consecutive nonpalpable breast cancers. AJR Am J Roentgenol 1986; 146:661-663.
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Sickles EA. Mammographic features of "early" breast cancer. AJR Am J Roentgenol 1984; 143:461-464.
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Douglas-Jones AG, Gupta SK, Attanoos RL, Morgan JM, Mansel RE. A critical appraisal of six modern classifications of ductal carcinoma in situ of the breast (DCIS): correlation with grade of associated invasive carcinoma. Histopathology 1996; 29:397-409.
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Silverstein MJ, Lagios MD, Craig PH, et al. A prognostic index for ductal carcinoma in situ of the breast. Cancer 1996; 77:2267-2274.
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Poplack SP, Wells WA. Ductal carcinoma in situ of the breast: mammographic-pathologic correlation. AJR Am J Roentgenol 1998; 170:1543-1549.
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Stomper PC, Margolin FR. Ductal carcinoma in situ: the mammographers perspective. AJR Am J Roentgenol 1994; 162:585-591.
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Winchester DJ, Menck HR, Winchester DP. National treatment trends for ductal carcinoma in situ of the breast. Arch Surg 1997; 132:660-665.
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Silverstein MJ, Lagios MD. Use of predictors of recurrence to plan therapy for DCIS of the breast. Oncology 1997; 11:393-410.
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Morrow M, Schnitt SJ, Harris JR. Ductal carcinoma in situ and microinvasive carcinoma. In: Harris JR, Lippman ME, Morrow M, Osborne CK, eds. Diseases of the breast. 2nd ed. Philadelphia, Pa: Lippincott Williams & Wilkins, 2000; 391-398.
Our congratulations to the 38 individuals who submitted the most likely diagnosis (ductal carcinoma in situ) for Diagnosis Please, Case 41. The names and locations of the individuals, as submitted, are as follows:
- Pablo J. Abbona, Mar del Plata, Argentina
- Gholamali Afshang, MD, Tinley Park, Ill
- Albert J. Alter, Madison, Wis
- Nabil Ammouri, MD, Zahle, Lebanon
- Philip A. Araoz, San Francisco, Calif
- R. James Brenner, MD, Santa Monica, Calif
- Michael P. Buetow, MD, Okemos, Mich
- Nelson M. G. Caserta, MD, Campinas, SP, Brazil
- Flavio Corti, MD, Mar del Plata, Argentina
- Dr. M. G. de Baets, Lugano, Switzerland
- Dra. Estela Di Nella, Mar del Plata, Argentina
- Julie El-Ferzli, Amiens, France
- Arie Franco, MD, PhD, Livingston, NJ
- Milton R. Fuentealba, MD, General Roca, Rio Negro, Argentina
- Gerrit Fund, MD, Ibbenbueren, Germany
- Dr. Shivanand Gamanagatti, New Delhi, India
- Douglas Gardner, Windsor, Ontario, Canada
- Burton M. Gold, MD, Mineola, NY
- Flavius Guglielmo, MD, Basking Ridge, NJ
- Marc J. Homer, MD, Boston, Mass
- Douglas S. Katz, MD, Mineola, NY
- Dr. Edward W. Kouri, Charlotte, NC
- S. Lachanis, MD, Athens, Greece
- Eduardo Lassalle, MD, Quilmes, Argentina
- Yoji Maetani, MD, Kyoto, Japan
- Frank McKowne, MD, Vancouver, Wash
- Sanford M. Ornstein, MD, Phoenix, Ariz
- Narendrakumar P. Patel, MD, Newburgh, NY
- Shawn P. Quillin, MD, Charlotte, NC
- Enrique Remartinez Escobar, MD, Melilla, Spain
- Luiz Antonio Rossi, São Paulo, Brazil
- Jami R. Rubens, MD, Concord, Mass
- Darrin S. Smith, MD, Tulare, Calif
- Arlene Sussman, MD, Mineola, NY
- Carlos Touma, Granada, Spain
- M. Wever-Koorevaar, Nijmegen, the Netherlands
- Joe Yut, Olathe, Kan
- Jeffrey H. Zapolsky, Oshkosh, Wis