Sebaceoma is a tumor for which the causative oncogenes are not well-understood. Sebaceomas demonstrate some histopathologic features similar to basal cell carcinoma (BCC), such as palisading borders and basaloid cells with additional features, including foamy cytoplasm and indented nuclei.We examine multiple cell-cycle, oncogene, and tumor suppressor gene markers in sebaceomas, to try to find some suitable biological markers for this tumor, and compare with other published studies.We investigated a panel of immunohistochemical (IHC) stains that are important for cellular signaling, including a cell cycle regulator, tumor suppressor gene, oncogene, hormone receptor, and genomic stability markers in our cohort of sebaceomas. We collected 30 sebaceomas from three separate USA dermatopathology laboratories. The following IHC panel: Epithelial membrane antigen (EMA)/CD227, cytokeratin AE1/AE3, cyclin D1, human breast cancer 1 protein (BRCA-1), C-erb-2, Bcl-2, human androgen receptor (AR), cyclin-dependent kinase inhibitor 1B (p27(kip1)), p53, topoisomerase II alpha, proliferating cell nuclear antigen, and Ki-67 were tested in our cases.EMA/CD227 was positive in the well-differentiated sebaceomas (13/30). Cyclin-dependent kinase inhibitor 1B was positive in tumors with intermediate differentiation (22/30). The less well-differentiated tumors failed to stain with EMA and AR. Most of the tumors with well-differentiated palisaded areas demonstrated positive staining for topoisomerase II alpha, p27(kip1), and p53, with positive staining in tumoral basaloid areas (22/30). Numerous tumors were focally positive with multiple markers, indicating a significant degree of variability in the complete group.Oncogenes, tumor suppressor genes, cell cycle regulators, and hormone receptors are variably expressed in sebaceomas. Our results suggest that in these tumors, selected marker staining seems to correlate with tumor differentiation; that is, well-differentiated tumors as a group stained with EMA and AR, and palisaded areas demonstrated consistent p53, topoisomerase II alpha and p27(kip1) staining. In contrast, less well-differentiated areas stained with a different spectrum of markers.
View details for DOI 10.4103/1947-2714.159338
View details for PubMedID 26199925