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)

Altogether 20 chordomas were reported. The site distribution included 9 cases at the sacrococcygeal region, another 9 cases at the spheno-occipital region, 1 at the cervical vertebra, and another 1 at the lumbar vertebra. Histologic examination revealed that characteristic "physaliphorous cells" were easily identified in all the 19 cases. Tissue for immunohistochemistry study was available in 18 cases. Among them, tumor cells were found strongly positive to EMA, but negative for CEA. 16/18 cases also showed positive for keratin and S-100 protein. Totally, 2 cases were studied ultrastructurally and there were abundant RER and microfilaments seen in the cytoplasm of the tumor cells but only few surface microvilli detected. The epithelial nature of chordoma is strongly supported by the ultrastructural and immunohistochemical findings of these 20 cases.
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PMID:[An immunohistochemical and ultrastructural study of 20 chordomas]. 137 90

Seventy-six cases of meningioma of various light microscopic features were studied immunohistochemically by using 6 kinds of antibodies directly against epithelial, mesenchymal and neural components. Except for hemangiopericyte meningiomas which only showed vimentin positive, expressions of vimentin and EMA were obtained in almost all the meningiomas. Thirteen meningiomas were investigated by electron microscopy. The electron micrograph of meningiomatous cell showed presence of interdigitation of the adjacent cell membrane with desmosome and variable amounts of intermediate filaments in cytoplasm, although the re were different varieties of cell types. 2 hemangiopericyte meningiomas showed presence of different ultrastructures, which contained many pericytes and cells with a large number of RER. These results provide evidences of the fact that meningioma possessed the features of both mesenchymal and epithelial tissue. In regard to histogenesis, findings reported suggest that meningioma most probably arise from the arachnoid cap cells. Additionally, some distinct subtypes of meningioma are reported, including secretory meningioma, microcystic meningioma and oncocytic meningioma.
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PMID:[An immunohistochemical and ultrastructural study on 76 cases of meningioma]. 263 60

Multinucleated giant stromal cells (MGSC) have been described in a variety of lesions of various anatomical sites. They are generally believed to be derived from fibroblasts or myofibroblasts. Their size and bizarre appearance may lead to an erroneous interpretation of infiltrating malignant cells, but they are regarded as reactive in nature. MGSC also seem to participate in a neoplastic process and form a part of tumors called giant cell fibroblastomas (GCF). In GCF, multinucleated giant cells are sparsely scattered throughout the tumor, which is composed of loosely arranged spindle cells. Thus far, no tumor composed of MGSC entirely, to the best of the authors' knowledge, has been reported. This study involved an 80-year-old female with an omental tumor, which is believed to represent the first case of tumor of MGSC. The patient developed abdominal pain; a large abdominal tumor measuring 18 x 15 x 5 cm by computerized tomography was found located between the left lobe of the liver, the transverse colon, and the greater curvature of the stomach. Although the tumor was adherent to the above organs and infiltrating the omentum, it was resectable. Grossly, the tumor was highly vascular and the surface was shaggy with no recognizable capsule. The cut surfaces were red to tan with frequent cystic spaces containing bloody material. Microscopically, the tumor cells were large and multinucleated (2-6 nuclei) with prominent nucleoli. The cytoplasm was abundant and stained amphophilic. These tumor cells formed moderately cellular sheets filling the spaces between the varying sized vessels. There was prominent vascularity throughout the tumor. DNA study by image analysis revealed aneuploidy peaks. On immunohistochemistry, the tumor cells were strongly positive for vimentin, moderately positive for actin along the periphery of the cytoplasm, and negative for cytokeratin, EMA, myoglobin, S-100, CEA, Factor XIIIa, HMB-45, and HAM56 and KP-1. Ultrastructurally, the cytoplasm contained rich profiles of RER with scattered lysosomes. The cell borders were slightly irregular with occasional subplasmalemmal densities facing loosely arranged collagenous stroma. The light microscopic, immunohistochemical, and electron microscopic features of tumor cells were remarkably similar to MGSC. The tumor size and gross appearance suggested a malignancy, but it was a diploid tumor and the patient remains disease free 5 years after a complete resection.
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PMID:Multinucleated giant stromal tumor of the omentum: report of a case with immunohistochemical and ultrastructural investigation. 878 15

We report a case of cellular neurothekeoma showing unusual immunohistochemical findings and occurring on the left upper arm of a healthy 48-year-old woman. She presented with a 1 cm, red, asymptomatic, dermal nodule of 1 year duration. A biopsy showed dermal proliferation of plexiform fascicles of spindle-shaped or polygonal cells with plentiful eosinophilic cytoplasms. The immunohistochemical profile included negative stains for S-100, CD34, factor XIIIa, CD68, HMB45, cytokeratins, and EMA, strongly positive stains for neuron specific enolase (NSE), synaptophysin, and chromogranin A, and focally positive ones for NKI/C3 and alpha-smooth muscle actin. Ultrastructural analysis showed undifferentiated mesenchymal cells with cytoplasmic projections and abundant RER. Although we couldn't find any confirmative cell type in this cellular tumor, we believe that cellular neurothekeoma is predominantly composed of undifferentiated cells that can exhibit features of neuroendocrine cells in addition to fibroblastic or myofibroblastic ones, suggesting a divergent cell origin.
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PMID:Cellular neurothekeoma with possible neuroendocrine differentiation. 1040 81

Invasive micropapillary carcinoma is associated with frequent lymph node metastasis and adverse clinical outcome. Initially described as a variant of breast and ovarian carcinoma, it has subsequently been found in other organs, most recently the colon. Reports of colorectal micropapillary carcinoma to date are limited in number, and their molecular profile has not been established. The aims of the present study were to analyze their clinicopathological features and molecular profile, and compare them with those of conventional adenocarcinoma. Clinicopathological features of a cohort of 379 patients with primary colorectal cancer were retrospectively reviewed for the presence of the pattern characteristic of micropapillary carcinoma. We also assessed the expression of KRT7, KRT20, CEACAM5, MUC1 (EMA, clone E29), MUC1 (clone MA695), MLH1, MSH2, MSH6 and TP53 by immunohistochemistry. Genetic assessments of microsatellite instability, chromosomes 17p and 18q, and mutations in TP53, BRAF and KRAS were performed using DNA extracted from formalin-fixed, paraffin-embedded sections. In all, 60 of the reviewed cases (16%) had a micropapillary component that ranged from 5 to 95% of the tumor, characterized by a higher frequency of an infiltrative pattern, lymphovascular and perineural invasion, a higher depth of invasion and more positive lymph nodes than conventional adenocarcinoma. Immunohistochemistry for MUC1 (clone MA695) and MUC1 (EMA, clone E29) enhanced the characteristic inside-out staining pattern of the micropapillary carcinoma component, whereas the rest of the tumor showed luminal staining patterns. KRT7 expression was slightly increased in micropapillary carcinoma, but did not reach significance (17-3%, P=0.1967). The molecular parameters showed a higher frequency of TP53 alterations and a low incidence of microsatellite instability and RER phenotype (loss of mismatch repair protein) in micropapillary carcinoma. With regard to the histological parameters, micropapillary carcinoma appears to be more aggressive than conventional colorectal adenocarcinoma. The molecular profile supports the hypothesis that micropapillary carcinoma carcinogenesis develops through the classical chromosomal instability pathway.
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PMID:Clinicopathological and molecular characterization of colorectal micropapillary carcinoma. 2133 62