title: Immunohistochemical staining for Ber-EP4, p53, proliferating cell nuclear antigen, Ki-67, bcl-2, CD34, and factor XIIIa in nevus sebaceus.
abstract: Increased expression of p53 has been found in the majority of basal cell carcinomas (BCCs). The pattern and intensity of this staining, as well as staining for proliferation antigens, seems to correlate with behavior of histologic subtypes of BCC. Nevus sebaceus (NS) is considered a hamartoma. Multiple epithelial neoplasms do arise in NS, and, rarely, they show an aggressive biologic behavior. Significant numbers of these neoplasms, however, have areas of basaloid hyperplasia that are often reported as BCC. Although morphologically similar to BCC, the mechanism underlying the development of these areas has not been investigated, so we sought to evaluate the expression of Ber-EP4, p53, proliferating cell nuclear antigen, Ki-67, bcl-2, Factor XIIIa, and CD34 in areas showing basaloid hyperplasia, arising in NS. We performed immunohistochemical stains for Ber-EP4, p53, proliferating cell nuclear antigen, Ki-67, bcl-2, Factor XIIIa, and CD34 on seven cases of NS with areas of basaloid hyperplasia. All of the eight cases of NS showed diffuse positive membrane staining for Ber-EP4 and negative nuclear staining for p53. Proliferating cell nuclear antigen and Ki-67 staining was only slightly increased in the areas of basaloid hyperplasia, compared with the surrounding epidermis and with areas of the epidermis peripheral to the hamartomatous proliferation, and bcl-2 was only focally positive. Factor XIIIa-positive cells and CD34-positive vascular endothelial cells were increased within the subjacent dermis, a pattern suggestive of follicular differentiation. Our findings suggest that even though areas of basaloid hyperplasia in NS are morphologically similar to BCC, they are induced by different stimulatory and molecular mechanisms. These different mechanisms result in expression of immunohistochemical markers more characteristic of benign follicular tumors than of BCC.
authors.affiliation: Naval Medical Center, San Diego, California, USA.
authors.forename: T L
authors.initials: TL
authors.lastname: Barrett
authors.forename: K J
authors.initials: KJ
authors.lastname: Smith
authors.forename: J
authors.initials: J
authors.lastname: Williams
authors.forename: S W
authors.initials: SW
authors.lastname: Corner
authors.forename: J J
authors.initials: JJ
authors.lastname: Hodge
authors.forename: H G
authors.initials: HG
authors.lastname: Skelton
mesh_terms: D000293:Adolescent; D000328:Adult; D018952:Antigens, CD34 / Q000378:metabolism; D000954:Antigens, Surface / Q000378:metabolism; D014408:Biomarkers, Tumor / Q000378:metabolism; D002648:Child; D003937:Diagnosis, Differential; D005260:Female; D006222:Hamartoma / Q000175:diagnosis / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D006965:Hyperplasia / Q000378:metabolism; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D018295:Neoplasms, Basal Cell / Q000175:diagnosis / Q000378:metabolism; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D009418:S100 Proteins / Q000378:metabolism; D012535:Scalp / Q000473:pathology*; D012871:Skin Diseases / Q000175:diagnosis / Q000378:metabolism* / Q000473:pathology; D012878:Skin Neoplasms / Q000175:diagnosis / Q000378:metabolism / Q000473:pathology; D011503:Transglutaminases / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D000951:Antigens, Neoplasm
chemical_list: D018952:Antigens, CD34; D000954:Antigens, Surface; D014408:Biomarkers, Tumor; D019394:Ki-67 Antigen; D018809:Proliferating Cell Nuclear Antigen; D019253:Proto-Oncogene Proteins c-bcl-2; D009418:S100 Proteins; D011503:Transglutaminases; D016159:Tumor Suppressor Protein p53; C115012:human epithelial antigen-125; D000951:Antigens, Neoplasm