Lipid cell (steroid cell) tumor of the ovary: immunophenotype with analysis of potential pitfall due to endogenous biotin-like activity.

Twenty-eight lipid cell (steroid cell) tumors of the ovary were studied by immunohistochemistry using an avidin-biotin complex detection system; 75% of tumors were vimentin positive, 46% were positive for cytokeratin (CAM5.2 antibody), 37% were positive with the cytokeratin cocktail AE1/AE3 and CK1, and 29% were positive for smooth muscle alpha-actin. Three tumors were positive for CD68 (KP-1), a histiocyte marker, and each of the following markers was positive in two cases: desmin, epithelial membrane antigen, neuron-specific enolase, and S-100 protein. All tumors tested were negative for chromogranin A, CD15 (Leu-M1), myoglobin, neurofilament protein, alpha-fetoprotein, carcinoembryonic antigen, and melanoma-associated antigen (HMB-45 antibody). Immunoreactivity for cytokeratins was usually focal, paranuclear, and globoid, while reactivity for actin and vimentin was diffuse and cytoplasmic. Based on these findings, melanomas and some carcinomas should be distinguishable from lipid cell tumors. However, the immunohistochemical profiles of smooth-muscle tumors, other gonadal stromal tumors (granulosa cell tumors, thecomas), and hepatocellular, renal cell, and adrenocortical carcinomas overlap with that of lipid cell tumors, and therefore these tumors may not be distinguishable from lipid cell tumors using this technique. In 10 cases (36%), negative controls exhibited weak to moderate nonspecific cytoplasmic staining. Evidence obtained using a biotin blocking kit, and a monoclonal antibody against biotin, suggests endogenous biotin-like reactivity as the source of the nonspecific staining.