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)

Lung carcinomas were studied immunohistochemically and the results were related to type of tissue sample (bronchoscopic biopsies, surgical specimens, autopsies). All cytokeratins (CAM 5.2, PKK-1, AE1/AE3) reacted with virtually all adenocarcinomas, most squamous, and 65% of the large cell carcinomas, while CAM 5.2 was most efficient with the small cell carcinomas. CEA stained 33% and 60% of the small and large cell carcinomas, respectively, most adenocarcinomas, and 84% of the squamous cell carcinomas, among which staining decreased with dedifferentiation and was often focal. EMA reacted with 90%, and NSE with 20% of all histological types. There was no staining for NF. All antibodies, except EMA, were more efficient with surgical specimens. Our study implies that the cytokeratins we used work better with surgical material, but are generally comparable to monospecific cytokeratin antibodies. Also, EMA is a reliable marker for epithelial differentiation with all types of tissue samples. Moreover, CEA negativity in several poorly differentiated lung carcinomas might have implications in the differential diagnosis against pleural mesothelioma.
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PMID:Immunohistochemical study of 158 lung carcinomas. 128 Jan 49

We report a primary choriocarcinoma of the urinary bladder in a 63-year-old man who presented with painless hematuria. He was diagnosed as having an invasive carcinoma and underwent a total cystectomy. The tumor was diffusely hemorrhagic and occupied the dome of the bladder. Histologically, it consisted of cyto-and syncytiotrophoblasts with extensive hemorrhage. No coexisting transitional cell carcinoma component was present. By immunohistochemistry, the tumor expressed beta-hCG and low-molecular weight cytokeratin intensely while it was negative for CEA or EMA. The post-cystectomy serum beta-hCG was 237mlU/ml, and decreased later. The pertinent literature is reviewed and diagnostic criteria are discussed.
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PMID:Primary choriocarcinoma of the urinary bladder--a case report. 129 42

Needle aspiration cytology, immunocytochemistry, and electron-microscopic findings are presented in three cases of an unusual pancreatic carcinoma in which pleomorphic giant cells formed an integral part of the tumour. All three patients were elderly males (age range 66-83 years) and had pancreatic masses. Notable cytologic features in all cases were the presence of bizarre mononucleated and multinucleated, poorly cohesive tumour giant cells, rare spindle cells, with occasional cannibalism and cytophagocytosis. Immunocytochemical study of aspirated material showed diffuse staining of cytokeratin and EMA within the tumour cells, while B 72.3 was seen as focal trace stain. Electron microscopy of aspirated material demonstrated epithelial features and these were characterised by the presence of tonofilaments and surface microvilli. Based on our findings, it is felt that the bizarre giant cells in this unusual variant of pancreatic carcinoma are of epithelial origin. The differential diagnosis of other tumours that may be associated with predominant giant cells in pancreatic aspirates is appropriately discussed.
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PMID:Needle aspiration cytology, immunocytochemistry, and electron microscopic study of unusual pancreatic carcinoma with pleomorphic giant cells. 139 30

Histological examination of a tumor centered in the body of the pancreas of a 65-year-old Iranian man revealed it to have a substantial component in which osteoclast-like giant cells were set within a stroma of pleomorphic mononuclear cells though other areas were composed of conventional adenocarcinoma. Immunocytochemistry was used to investigate the differentiation of the various component cells of the tumor. The carcinoma cells of the usual type expressed epithelial antigens (EMA and cytokeratin). The giant cells expressed vimentin and showed membrane staining with anti-LCA, in common with examples of cells originating from the mononuclear phagocytic system, including normal osteoclasts. The accompanying stromal cells expressed vimentin only. This implies that the giant cells are likely to have their origin in the bone marrow, whereas the mononuclear stromal cells that separate them may represent tumor cells that have lost their epithelial phenotype. The giant cells are therefore an unusual tissue response to the presence of the carcinoma.
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PMID:Adenocarcinoma of the pancreas with osteoclast-like giant cells: a case report with immunocytochemistry. 151 8

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

Most compensations for asbestos-related deaths secondary to cancer center around mesothelioma and bronchogenic carcinoma. The differential diagnosis between mesothelioma and adenocarcinoma is a common and troublesome one, necessitating the correlation between clinical history, radiographic findings, and pathologic examination of tissues and cells. We describe a multimodal approach based on the use of routine and special stains, immunocytochemistry, and electron microscopy for distinguishing between mesothelioma and adenocarcinoma. Once a malignant diagnosis is arrived at by careful pathological examination, the tumor is classified as mesothelioma if mesothelial cells are identified as the constituent cells of the neoplasm. Mesothelial cells are recognized by (1) their main ultrastructural features: slender and elongated microvilli, abundant intermediate filaments, and lacking secretory granules; and (2) their characteristic immunocytochemical reactivity: positivity for cytokeratin, EMA, and vimentin, and negativity for carcinoembryonic antigen (CEA), B72-3, Leu-M1, and other gland-cell markers. A variety of methods have been attempted in an effort to distinguish between reactive and malignant mesothelial cells. In practice, however, such distinction depends more on experience and expertise than in any fool-proof ancillary tests. A number of these tests are discussed along with the illustration of classical and unusual examples of mesothelioma and other pleural tumors.
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PMID:Differential diagnosis between mesothelioma and adenocarcinoma: a multimodal approach based on ultrastructure and immunocytochemistry. 160 55

64 diffuse pleural mesotheliomas diagnosed between 1964 and January 1985 at the Institute of Pathology of the University of Freiburg were analyzed. Since 1980 an increase from one case to 10 cases per year has been observed. The tumor was 3 to 4 times more frequent in men than in women. The age distribution showed a peak between the age of 50 and 60. In 26 cases evidence of exposure to asbestos was detected. In one patient radiotherapy of Hodgkin's disease may have been of etiological significance. The median survival time was 13 months. The five-year survival rate was only 4%. Histologic reevaluation was only possible in cases diagnosed after 1975. Of 43 cases thus evaluated 26 were pure mesothelial, 15 biphasic and 2 of the spindle-cell subtype. A median survival time of 23 months for pure mesothelial mesothelioma in comparison to 13 months for the biphasic mesothelioma indicated a better prognosis for pure mesothelial mesothelioma. Although no other primary tumors were detected, in 10 cases the differential diagnosis of adenocarcinoma had to be considered, and in 3 cases tumors of non-epithelial origin had to be excluded. 35 of 43 mesothelioma were CEA-negative, 38 out of 43 cytokeratin-positive, and 33 out of 43 were EMA-positive. Factor-VIII-related antigen was not demonstrated. 12 of 43 mesotheliomas showed PAS-positive staining, 29 of 43 were stained with Alcian blue. 7 of these 29 showed a positive digestion with hyaluronidase. Although CEA may not be negative in every mesothelioma, this marker seems to be a valid tool for the differential diagnosis of adenocarcinoma. In order to safeguard against a mistaken diagnosis of pleural mesothelioma, the exclusion of other tumors is always indispensable.
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PMID:Malignant pleural mesothelioma: some aspects of epidemiology, differential diagnosis and prognosis. Histological and immunohistochemical evaluation and follow-up of mesotheliomas diagnosed from 1964 to January 1985. 169 Apr 13

The present study is based on the histopathological and immunohistochemical examination of seven chondroblastomas, including one lung metastasis occurring 9 years after treatment. Chondroblastomas were shown to co-express vimentin, S-100 protein, neuron-specific enolase, and the epithelial markers recognized by CAM 5.2, EMA and a polyclonal cytokeratin antibody. The cytokeratins present in the tumour cells of the lung metastasis were characterized as cytokeratins 8, 18, 19 and, to a lesser extent, cytokeratin 7. The results suggest aberrant cytokeratin expression in chrondroblastomas.
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PMID:Cytokeratin expression in chondroblastomas. 169 5

True malignant mixed tumor (TMMT) of salivary glands, with both carcinomatous and sarcomatous components, is exceedingly rare. We offer a case of TMMT in a 79-yr-old man, which may represent the first report example of this unusual neoplasm arising in the tongue. The carcinomatous component was mainly of solid basaloid carcinoma with focal glandular differentiation, while the sarcomatous component was composed of pleomorphic elements such as chondrosarcoma, myxosarcoma and fibrosarcoma. Carcinoma cells at the periphery of solid nests occasionally merged into these sarcomatous elements. Immunohistochemically, basaloid carcinoma cells showed positive reaction for both low molecular weight cytokeratin and S-100 protein, whereas carcinoma cells lining ductal spaces were positive for a wide spectrum of keratin and EMA. The sarcomatous elements revealed the presence of vimentin and S-100 protein. Ultrastructurally, basal lamina-like material and/or mucoid precipitates often accumulated separating the tumor cells from each other singly or into a few cell group. Some sarcomatous cells assumed the myoepithelial features, such as the presence of microfilament bundles with dense bodies and pinocytotic vesicles along the cell periphery. These findings may indicate that TMMT shares a common histogenesis with pleomorphic adenoma.
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PMID:Ultrastructural and immunohistochemical observations of a true malignant mixed tumor (carcinosarcoma) of the tongue. 169 22

The cytologic diagnosis of malignancy in serous effusions can be challenging. An immunocytochemical (ICC) panel using commercially available antibodies (to carcinoembryonic antigen [CEA], epithelial membrane antigen [EMA], B72.3, Leu-M1, cytokeratin [CK], leukocyte common antigen [LCA], S-100 protein, and vimentin) was applied to cell blocks fixed in methyl Carnoy's solution that were from 55 consecutive pleural, peritoneal, and pericardial fluid specimens. The results were correlated with data from clinical records and routine cytologic studies. Final cytologic diagnoses included 26 of adenocarcinoma and 1 of mesothelioma. The remaining 28 cases were considered to be benign (reactive) proliferations. EMA, CEA, B72.3, and Leu-M1 were present in 96%, 77%, 58%, and 42% of adenocarcinomas, respectively. These determinants were absent in the mesothelioma and the reactive effusions, although anti-CEA yielded strong background staining of inflammatory cells. The CK markers identified malignant cells in 93% of cases, but consistently stained mesothelial cells as well. Antivimentin strongly labeled mesothelial cells in all cases, with weak to absent staining of malignant cells. In 3 of 26 carcinoma cases (12%), the ICC panel identified malignant cells that were not recognized initially on routine cytologic examination. In 1 of 26 cases (4%), the panel was falsely negative. Use of this approach can improve the diagnostic accuracy of cytologic examination of serous fluids. The ICC panel is especially helpful when atypical mesothelial proliferation is present, or in cases that are clinically suspect for malignancy, but cytologically negative because there are only a few malignant cells, or those that are cytologically bland.
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PMID:Immunocytochemical panel for the identification of malignant cells in serous effusions. 171 Apr 19


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