An immunohistochemical study of the breast using antibodies to basal and luminal keratins, alpha-smooth muscle actin, vimentin, collagen IV and laminin. Part II: Epitheliosis and ductal carcinoma in situ.

A detailed immunohistochemical study has been carried out on 63 breast lesions with epitheliosis, ductal carcinoma in situ and clinging carcinoma (lobular cancerization), using antibodies directed against keratins 5/14 and 14, 15, 16, 18, 19, vimentin, smooth muscle actin, collagen IV and laminin. The results have shown that epitheliosis on the one hand and ductal in situ and clinging carcinoma on the other are immunohistochemically different epithelial lesions. Epitheliosis appears to be epithelial hyperplasia with keratin 5/14 and keratin 14, 15, 16, 18, 19-positive cells. Compared to epitheliotic cells tumor cells of clinging carcinoma, lobular cancerization and ductal carcinoma in situ expressed only luminal keratins 14, 15, 16, 18, 19 in 85% of the cases studied; whereas in 15% there was a basal keratin expression. From our results we conclude that the clinging carcinoma (lobular cancerization) represents the initial morphological step in the development of ductal carcinoma in situ and thus may be interpreted as a minimal ductal neoplasia. With the immunohistochemical demonstration of basal and luminal keratins it may be possible in individual cases to differentiate between benign and malignant in situ lesions of the breast.

An immunohistochemical study of the breast using antibodies to basal and luminal keratins, alpha-smooth muscle actin, vimentin, collagen IV and laminin. Part I: Normal breast and benign proliferative lesions.

The distribution of simple epithelial (K8/18/19) and basal (myoepithelial) (K5/14) keratins, alpha-smooth-muscle actin, vimentin, collagen IV and laminin in normal mammary glands and in benign proliferative lesions was studied using monoclonal antibodies (mAbs). These antibodies (Abs) identified myoepithelial cells and luminal cells specifically. In lesions with adenosis and papillomas, the two-layered formation resembled that of normal glands with a purely myoepithelial-epithelial differentiation. In scleradenotic lesions, the main cell was of myoepithelial immunophenotype with intermixed trabecular-tubular proliferations of simple-type epithelium. The sclerosis seems to be the result of an irregular basal lamina synthesis by the myoepithelial cells. In contrast to these lesions, epitheliosis represents a purely intraluminal cell proliferation of clearly simple epithelial immunophenotype and of cells with a basal keratin phenotype, lacking myoepithelial differentiation antigen actin. The basal keratin type epithelium may represent post-stem or intermediate cells developing into luminal epithelium. Epitheliosis appears to be a purely epithelial hyperplasia with striking similarity to the regeneration of normal breast epithelium. The different proliferative patterns may give an explanation for differences in potential cancer risks of patients with these lesions.