Sclerosing lesions Some benign breast processes are characterised by a combination of epithelial proliferation, with or without a myoepithelial component, and stromal fibrosis and sclerosis which may result in formation of a mass lesion. The entities which can be placed within the umbrella of sclerosing lesions are sclerosing adenosis (SA), microglandular adenosis (MGA) and radial scar/complex sclerosing lesion (RS/CSL). They have many overlapping features and may all give rise to diagnostic problems clinically, on imaging (ultrasound and mammography) and histopathologically. Although they are frequently impalpable, both sclerosing adenosis and complex sclerosing lesion may produce palpable masses which can easily be mistaken for invasive carcinoma. Fine microcalcification is a common feature of all three entities and the appearances on mammography may be closely similar to those of low grade ductal carcinoma in situ (DCIS). 9 In addition both SA and RS/CSL may be identified on mammography or ultrasound as an architectural distortion or spiculate mass which cannot be distinguished with confidence from carcinoma. In all these situations a tissue diagnosis must be established and increasingly this is obtained pre-operatively through needle core biopsy using one of the new spring loaded guns. 10-12 Diagnostic difficulty may be experienced histopathologically in interpreting such samples, and indeed in some circumstances excision biopsy specimens may also cause problems, the main differential diagnosis being invasive carcinoma, especially of tubular type. The main morphological features of the sclerosing lesions and tubular carcinoma are shown in Table 2. Sclerosing adenosis is characterised by a disorderly proliferation of acinar and ductular epithelial cells, myoepithelial cells and intralobular stroma which results in expansion and distortion of lobules and an overall whorled appearance. Despite the apparent disorganisation of the cellular proliferation a lobulocentric architecture is maintained. The epithelial component may form microtubular structures but the compressed acini frequently show obliteration of their lumina. Nuclei are small and regular without atypia and mitotic figures are infrequent. Fine foci of microcalcification are frequently found within the lumina of epithelial structures. In microglandular adenosis there is a disorderly proliferation of small round acinar structures, apparently infiltrating between normal ducts and lobules and extending into adipose tissue. There is no spindle cell proliferation and the growth pattern is not lobulocentric. The acini appear to be lined by a single layer of epithelial cells and the lumina often contain PAS positive, diastase-resistant, eosinophilic material which may, rarely, be calcified. Classically radial scar/complex sclerosing lesions are composed of a radial arrangement of ductular structures around a central fibroelastotic core. In early lesions the central connective tissue is cellular and includes numerous myofibroblasts. The entrapped ductular or tubular structures are lined by a two-layered epithelium although epithelial proliferation is commonly present. Atypical ductal hyperplasia or lobular neoplasia may also be seen. 13 As noted above the most important differential diagnosis for all these lesions is invasive carcinoma, especially the tubular type. In excision specimens sclerosing adenosis can usually be distinguished by its circumscribed lobulocentric low power morphology in contrast with the infiltrative pattern and desmoplastic stroma of tubular carcinoma, but care should be taken with needle core and frozen section specimens in which this feature may not be apparent. Furthermore, the architectural distortion produced in both these techniques may result in a mistaken diagnosis of infiltrating lobular carcinoma due to compression of the epithelial structures. In rare cases of sclerosing adenosis extension of the glandular components into perineural and vascular spaces is seen, a finding that must not be regarded as indicative of malignancy in the absence of confirmatory features. The presence of apocrine atypia may also raise the question of malignancy 14 and this should be avoided by recognition of the benign features described above. Both ductal carcinoma in situ and lobular neoplasia have been recorded in the nodular form of sclerosing adenosis and may be mistaken for invasive carcinoma if the presence of myoepithelial cells is not recognised. 15 If the diagnosis is in doubt immunostaining with anti-smooth muscle actin will readily demonstrate their presence, thus excluding the diagnosis of invasion. Microglandular adenosis can usually be distinguished from tubular carcinoma by its diffuse pattern and lack of central elastosis and desmoplastic stroma, although the sclerosing type of tubular carcinoma may provide a close mimic. A useful distinguishing feature is the fact that the glandular structures in MGA are usually uniform and rounded in contrast with the less regular, often angulated appearance in tubular carcinoma. Immunostaining for anti-smooth muscle actin is less helpful in MGA because in most recorded cases myoepithelial cells are said to be absent. 16, 17 MGA may also be confused with the tubulo-lobular variant of infiltrating lobular carcinoma. However, careful examination in the latter always reveals cords of cells typical of the classical lobular type in addition to microtubular structures. In the great majority of cases of RS/CSL the distinction from tubular carcinoma is relatively straightforward. The dense, sclerotic, poorly cellular stroma and elongated flattened tubules are quite different from the desmoplastic stroma and well formed oval structures in tubular carcinoma. However, more complex lesions with an admixture of sclerosing adenosis and epithelial hyperplasia may cause problems; it must also be remembered that both in situ and invasive carcinoma may be encountered in association with RS/CSL. 13 If there is any doubt about the correct diagnosis immunostaining with anti-smooth muscle actin will help to clarify both these problems. Great care should be taken in the interpretation of sclerosing lesions found on needle core biopsy because of the sampling problem. For example, the finding of part of a benign RS/CSL on core biopsy does not exclude the possibility of associated malignancy; it is, therefore, still our policy to excise all parenchymal distortions or architectural deformities. |
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