Basaloid/follicular hyperplasia overlying connective tissue/mesenchymal hamartomas simulating basal cell carcinomas

Background: Basaloid hyperplasia has been described overlying dermatofibrom as as well is in the epidermis overlying nevus sebaceus. Although the morph ology of these areas may resemble-that of basal cell carcinoma (BCC), in th e majority of cases aggressive behavior of the proliferation is not seen. I n fact, the basaloid proliferation often shows follicular differentiation a nd may be stimulated and maintained by its relationship with the underlying stromal cells. Objective: We wanted to determine whether immunohistochemical staining for antibodies, which may suggest differences in pathogenesis, were different i n basaloid hyperplasia overlying connective tissue/mesenchymal hamartomas a nd BCC. Methods: We report 3 cases of connective tissue/mesenchymal hamartomas with overlying basaloid hyperplasia, in which the areas of the basaloid prolife ration showed Follicular differentiation. Immunohistochemical stains includ ed Ber-EP4 PCNA, Ki-67, Bcl-2, p53, SM-Actin, CD31, Factor XIIa, KP-1, and CD34. Results: There was a diffuse positive reaction for Ber-EN in all specimens and there was increased nuclear staining for PCNA and Ki-67. There was foca l cytoplasmic staining for Bcl-2 in the areas of basaloid hyperplasia. Immu nohistochemical staining for p53 showed only scattered positive cells excep t in a small focus in the areas of basaloid hyperplasia. The connective tis sue component of all lesions showed diffuse staining for CD34 surrounding a reas of basaloid hyperplasia in the mesenchymal component as well as in abu ndant S-100(+) nerves. Conclusion: The areas of basaloid hyperplasia in these hamartomas exhibited an immature phenotype similar to that seen in both BCCs and follicular tum ors; however, the patterns of proliferation markers, p53, Bcl-2, and the su rrounding stromal cell markers were similar Lo those of benign follicular t umors. Thus the staining pattern for this group of antibodies suggests that areas of basaloid hyperplasia are not BCC.