Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0268596 (EMA)
 2,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gliosarcomas are mixed tumors with malignant glial and mesenchymal elements. The number of GFAP-positive tumor cells decreases with the increase of sarcomatous components, until whole areas may be GFAP negative. These distinct differentiations may, however, lead to false interpretations in small tissue samples. In this connection, it is of interest that, according to other reports, glial tumors may be positive for different anti-keratin antibodies and this prompted us to undertake a systematic investigation of the immunoreactivity of gliosarcomas using a panel of well-characterized monoclonal antibodies against cytokeratins (KL1, AE 1/3, Lu-5, CK-19, CK MNF 116 and Ma-903). These cases were further studied with the anti-epithelial non-cytokeratin antibodies EMA, HEA 125, Ber-EP4, CEA as well as the melanoma-antibody HMB-45, Leu-M1, GFAP and vimentin. As screening study we examined 20 cerebral metastatic carcinomas, 21 malignant gliomas (including 6 gliosarcomas) and 3 metastatic melanomas with the monoclonal antibodies KL1 and HMB-45. All cerebral metastatic carcinomas and 4/6 gliosarcomas were positive for KL1, whereas all melanomas, 2 metastatic carcinomas and 3 gliosarcomas showed an immunostaining with HMB-45. All gliosarcomas were positive with at least one of the tested anti-cytokeratin antibodies. The gliosarcomas did not show an immunoreaction in any of the cases when CEA, HEA 125, Ber-EP4, EMA or Leu M1 were applied. In our opinion, the monoclonal antibodies HEA 125 and Ber-EP4 could obviously be helpful in differentiating gliosarcomas from metastatic carcinomas.
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PMID:Epithelial and melanoma antigens in gliosarcoma. An immunohistochemical study. 159 90

We report a case of gliosarcoma with numerous giant cells resembling ganglion cells and having clear nucleoli. A 75-year woman was admitted to our hospital suffering from progressive left hemiparesis and ambulatory disturbance of one week's duration. CT and MRI studies showed ring enhancement on a clear margin mass in the right parieto-occipital lobe. The mass was totally removed macroscopically. Her left hemiparesis had improved and self walk came to be possible. But the tumor was regrowthed during next two months and she died for three months and a week. The gross and microscopic appearances of the tumors showed the double structure. The surface of the tumor was well enhanced and consisted of soft, gray, and easily bleeding tissue. The central core, however, was poorly enhanced and consisted of hard, yellow, non-bleeding tissue. Macroscopically, the central area included numerous giant ganglion-like cells which were negative for GFAP but positive for EMA in the cytoplasm. These giant cells had abundant collagen fibers and were surrounded by such fibers. Microscopic findings of the surrounding area included numerous spindle shaped cells which were positive for GFAP and vimentin. The origins of giant cells or tumor tissues have long been discussed, but no consensus has yet been obtained. Therefore, we speculated as to the origin in our patient based on immunohistochemical study and the findings of electronmicroscopy. We concluded, in sharp contrast to the old theory of one origin, epithelial tissue of a hamartomatous nature existed initially, followed by the growth of malignant tissue of a reactive astrocytic tumor with a sarcomatous component.
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PMID:[A case of giant cell-rich gliosarcoma]. 936 93

By analogy to gliosarcoma, the term "ependymosarcoma" has recently been coined to thematize the rare phenomenon of a malignant mesenchymal component arising within an ependymoma. We report on an example of this paradigm, involving tanycytic ependymoma as the host tumor in a 40-year-old female who underwent two tumor extirpation procedures at one-year interval. She first presented with severe headaches, and was seen by imaging to harbor a moderately enhancing mass 2.5cm in diameter at the rostral septum pellucidum accompanied by occlusive hydrocephalus. Microscopically, the tumor consisted of solid, wavy fascicles of elongated cells that were occasionally interrupted by vague perivascular pseudorosettes. Mitotic activity was absent, and less than 1% of nuclei immunoreacted for MIB-1. A histological diagnosis of tanycytic ependymoma (WHO grade II) was rendered, and no adjuvant therapy given. At recurrence, the lesion was 3.5cm in diameter, intensely enhancing, and had already seeded into the subarachnoid space. Histology showed a biphasic glial-sarcomatous architecture with remnants of the original ependymoma now displaying hypercellularity and atypical - yet not frankly anaplastic - features. The sarcomatous moiety consisted of spindle and epithelioid cells densely interwoven with reticulin fibers. While the ependymal component was GFAP and S100 protein positive, and featured punctate staining for EMA, none of these markers was expressed in the adjacent sarcoma. Instead, the latter reacted for vimentin and smooth muscle actin. To the best of our knowledge, this is the first documentation of tanycytic ependymoma undergoing malignant transformation, one driven by a highly anaplastic mesenchymal component, corresponding to "ependymosarcoma".
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PMID:Rapid spontaneous malignant progression of supratentorial tanycytic ependymoma with sarcomatous features - "Ependymosarcoma". 1985 84

The authors report a rare a case of gliosarcoma metastases in a 28-year-old male patient. The cauda equina roots were involved after brain tumor 16 months ago, which, on microscopic study, had a biphasic pattern and heterogeneous staining in the reaction with antibody to GFAP and vimentin; the tumor cells did not express EMA, EA, and desmin. Gliosarcoma was diagnosed, by taking into account morphological and immunohistochemical data. Tumor tissue of the cauda equine roots had the same immunophenotype as the brain tumor with a predominance of glial component, which permitted the source of metastases to be ascertained.
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PMID:[Multiple gliosarcoma metastases in the cauda equina roots]. 2108 41