Two mesothelioma samples from which the tumor cells could be obtained free of other cell types were found to contain vimentin as well as simple epithelial keratins and to synthesize these same proteins during short-term culture.
A mixed mesenchymal-epithelial phenotype, defined by reactivity with antibodies to epithelial membrane antigen and to vimentin and keratin intermediate filaments, was found in the tumor, and a similar phenotype persisted in the cultured cells.
Immunohistochemically, the original tumor had exhibited an intriguing potential for multidirectional differentiation with features of mesenchymal, epithelial and neural differentiation, evidenced by the co-expression of vimentin, cytokeratins and neurofilament proteins, respectively.
Immunostaining revealed that the tumors were positive for S-100 protein and vimentin and negative for glial fibrillary acidic protein, actin, and keratin.
Strong immunohistochemical staining for glial fibrillar acidic protein was demonstrated, while vimentin, neurofilament, and S-100 protein were all positive in just the astrocytic part of the tumor.
Both cell lines exhibited tumor cell morphology and growth kinetics and showed variable expression of glial fibrillary acidic protein (GFAP), S-100, fibronectin and vimentin.
For comparison with reg, alpha-1-antitrypsin (AAT), lysozyme, chromogranin A (CMG), CA 19-9, carcinoembryonic antigen (CEA), cytokeratin, vimentin, and alpha-fetoprotein (AFP) were assessed in those tumors.
Immunohistochemically, all SpCCs were positive for at least one of the epithelial markers (epithelial membrane antigen, nine cases; AE1/AE3, nine cases; carcinoembryonic antigen, three cases; and EAB 903, one case), and the tumor cells also were immunoreactive to mesenchymal marker (vimentin, eight cases), muscle markers (alpha-smooth muscle actin, one case; desmin, one case), and histiocytic marker (HAM 56, one case).
A total of 30 sex cord-stromal tumors including 9 adult type and 5 juvenile type granulosa cell tumors (GCTs), 4 Sertoli-Leydig cell tumors (SLTs), 1 gynandroblastoma, 5 thecomas, 2 fibromas and 3 sclerosing stromal tumors were immunohistochemically evaluated by means of cytokeratins of different molecular weight, vimentin and laminin with regard to the histogenesis of these tumors and to the embryogenesis of the sex cord and stroma of developing gonads.
Okadaic acid bound to a catalytic subunit of PP-1 and PP-2A and induced hyperphosphorylation of proteins, such as vimentin, cytokeratins, HSP 27, and tumor suppressor gene products.
Immunohistochemically, the paraffin-embedded tumor tissue displayed positive vimentin reactivity and lack of cytokeratin expression, indicating a mesenchymal origin.
Our results suggest that one of the roles of PEA3 in mammary tumor is to participate the activation of vimentin gene whose gene product in turn contributes to the metastatic potential of mammary tumors.
Immunofluorescence data show a decrease in the percentage of GFAP-expressing cells with increasing in vitro passages but a full reexpression (100% of GFAP-positive cells among vimentin-positive cells) was observed in cultures just derived from the xenotransplanted tumor.
Despite the marked morphologic resemblance of these tumors to high-grade sarcomatoid renal cell carcinoma, their phenotype (HMB45+, CD68+/-, actin+/-, and vimentin and keratin negative) is in contrast to that observed in epithelial tumors and parallels the phenotypic profile of angiomyolipoma.
Tumor cells were usually reactive with antibodies to keratin (67 of 78 cases, 86%), epithelial membrane antigen (50 of 54, 93%), vimentin (64 of 66, 97%), desmin (70 of 78, 90%), neuron-specific enolase (60 of 74, 81%), and the EWS-WT1 chimeric protein (25 of 27, 93%); typically nonreactive for muscle common actin (one of 58, 2%), myogenin (zero of eight, 0%), and chromogranin (one of 46, 2%); and variably reactive for MIC2 (nine of 47, 20%) and p53 (five of 17 with > 20% tumor cells reactive).