Columnar Alteration With Prominent Apical Snouts and Secretions : A Spectrum of Changes Frequently Present in Breast Biopsies Performed for Microcalcifications

A total of 10,542 breast biopsy specimens obtained between 1950 and 1968 were studied. Examples of atypical "ductal" (ADH) and atypical lobular hyperplasia (ALH), defined as having only some features of carcinoma in situ (CIS), were diagnosed in 3.6% of these specimens. In the same series, CIS was diagnosed in 1.7% of biopsy specimens excluding those with invasive cancer. The subsequent risk of invasive breast carcinoma after ALH or ADH was 4-5 times that of the general population. Follow-up was 90% successful and extended 17 years after biopsy. History of breast cancer in a mother, sister, or daughter doubled the risk of subsequent invasive carcinoma development (to 8 times for ALH and 10 times for ADH). The authors conclude that among the epithelial hyperplastic lesions of the human breast, a minority may be recognized by their resemblance to CIS which have a clinically significant elevation of subsequent breast cancer risk. This risk is one-half that of CIS.

Small ectatic ducts lined by atypical ductal cells with apocrine snouts occasionally have been observed in association with tubular carcinoma; some pathologists have considered these carcinomas to be a form of ductal carcinoma in situ (DCIS). Thirty-two cases of tubular carcinoma, 41 of invasive grade 1 ductal carcinoma with DCIS, 40 of invasive grade 1 ductal carcinoma without DCIS, 40 of invasive grade 3 ductal carcinoma, 40 of invasive lobular carcinoma, 20 of well-differentiated DCIS, and 80 of fibrocystic changes were examined to determine the relationship between the lesion formed by atypical ductal cells with apocrine snouts and invasive carcinoma, DCIS, and benign breast changes. Seventeen cases contained lesions formed by atypical ductal cells with apocrine snouts: 14 were associated with tubular carcinoma (43.7%), and 3 with invasive grade 1 ductal carcinoma (3.7%). In six invasive carcinomas, the associated DCIS was formed by cells identical to those within the lesion. These lesions were found at the periphery of the invasive carcinoma and adjacent to the DCIS. The lesions were probably composed of low-grade intraductal malignant epithelial cells, which partially involve small ectatic ducts and are often adjacent structures as a form of cancerization. This cytologic and architectural form of DCIS appears to be related to an invasive carcinoma that is usually of tubular subtype. Attention to this form of cancerization by malignant intraductal cells, especially with regard to specimen surgical margins, is imperative when a tubular carcinoma is encountered. If a pathologist encounters only this lesion in a partially sampled breast biopsy specimen, additional (or all) tissue should be submitted for histologic evaluation to ensure that an invasive carcinoma is not missed. This lesion needs to be distinguished from the frequent, benign, columnar alteration within lobules and small ectatic ducts.