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)

To date, one hundred and ten cases of malignant neoplasms arising from untreated bladder exstrophy have been reported. We describe another case of uncorrected bladder exstrophy with invasive adenocarcinoma and in situ squamous carcinoma discovered in a 51 year old woman. Postoperative radiotherapy was performed after cystectomy with nephroureterectomy and hysterectomy. The neoplastic samples were investigated by mucin histochemistry and immunocytochemistry. The epithelium lining the tumor villi and the surrounding mucosae was colonic with mucin histochemistry and reacted to anti KL1, EMA and ACE antibodies. These features were those of colonic and vesical adenocarcinomas. Although early vesical reconstruction is the best oncologic prevention, patients with bladder exstrophy run the risk of sigmoid adenocarcinoma after cystectomy and urinary diversion including ureterosigmoidostomy.
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PMID:[Invasive adenocarcinoma with epidermoid carcinoma on the site of bladder exstrophy. Histochemical and immunocytochemical study]. 178 47

We have cloned the Muc1 gene of the mouse, encoding the murine equivalent of human episialin (also known as EMA or PEM), a mucin-like glycoprotein that is overexpressed in carcinoma cells. The extracellular domain of the mouse protein, that mainly consists of tandem repeats, contains 16 repeats of variable length and sequence, whereas the human protein usually contains between 30 and 90 nearly identical repeats. The murine repeats contain more potential O-glycan side chains and this may result in a more extended conformation of the murine protein. The transmembrane and cytoplasmic domains of the protein show about 90% conservation. The promoter region shows many conserved regions that could function as transcription factor binding sites.
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PMID:The mouse episialin (Muc1) gene and its promoter: rapid evolution of the repetitive domain in the protein. 195 79

Fourteen cases of extramammary Paget's disease and five cases of mammary Paget's disease have been studied using stereomorphometric, histochemical, and immunohistochemical methods. The antibodies were anti-CEA, anti-EMA, 115D8 and DF3. Intracytoplasmic mucin was positive in Paget's cells, and both 115D8 and DF3 were detected intensely in all of Paget's cells. 115D8 and DF3 were also positive in the normal apocrine sweat gland, the intercellular canaliculi of the eccrine sweat gland, and the intraductal carcinoma of the breast. Therefore, we have concluded that extramammary Paget's disease is an intraepidermal adenocarcinoma originating in the apocrine sweat gland.
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PMID:[An immunohistochemical analysis of extramammary Paget's disease compared with mammary Paget's disease]. 283 11

Light microscopic, immunohistochemical and ultrastructural studies were performed on a surgically removed left atrial myxoma containing glandular structures. Routine examination showed glandular lumina lined by cylindric epithelium in the characteristic myoxoid stroma, and the glands contained PAS positive mucin. The glandular structures demonstrated significant positivity for wide-spectrum-CK, EMA, and moderate positivity for CEA. Stromal cells were positive for vimentin, FVIII. Ag was present only in surface cells and blood vessels. Ultrastructurally the gland showed characteristics of mucin secreting epithelium. The authors briefly overview the currently existing theories about the histogenesis of myxomas.
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PMID:[Glandular myxoma of the heart]. 759 93

Hepatoma cases (n = 130) were analyzed by means of histochemical and immunohistochemical stainings. There were 99 cases of hepatocellular carcinoma (HCC), 15 cholangiocarcinoma (CC), and 16 combined HCC and CC (HCC+CC). The clinical features and the cases accompanied with hepatitis and/or liver cirrhosis in the non-tumor liver tissue of HCC+CC cases were intermediate between HCC and CC cases. Histologically, in HCC+CC cases, there were 4 cases with trabecular, 4 with pseudoglandular, 3 with solid type. In these 11 cases, the CC occupied less than 10% of the neoplasm. These cases were designated as HCC+CC type I. There was no obvious stromal fibrosis. The rest 5 cases of HCC+CC cases showed tubular carcinoma in which the CC occupied more than 10% of the tumor. These cases were designated as HCC+CC type II. There was significant fibrosis in the stroma. In all HCC+CC cases only the CC region was positive for mucin and EMA staining. Nearly 70% of the HCC+CC cases had intracytoplasmic glycogen in the HCC area. Transition areas between HCC and CC in both type I and type II HCC+CC cases were observed and they were mucin negative but EMA positive. In conclusion, HCC+CC has both HCC and CC regions with the characteristics of HCC and CC, respectively. Histochemical mucin staining and immunohistochemical EMA staining are helpful in the detection and diagnosis of the HCC+CC.
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PMID:[Clinicopathologic features and diagnosis of mixed type hepatocellular carcinoma]. 765 28

In a randomized design we examined the interobserver variation in the histopathological diagnosis of adenocarcinoma of the lung and malignant mesothelioma. In three rounds, three pathologists assessed slides from 42 tumours originally diagnosed as adenocarcinomas, malignant mesotheliomas or benign lesions in the pleura. In the first round the assessments were made on haematoxylin and eosin (H & E) stained sections; in the second, on H & E sections plus sections stained with histochemical mucin stains; and in the final round, the diagnoses were made on H & E sections and sections stained with a panel of antibodies against various antigens (cytokeratin, EMA, CEA, Ber-EP4, B72.3, Leu-M1, vimentin and S-100 protein) said to be of value in the differential diagnosis. The overall interobserver agreements for the three rounds were 0.659, 0.802 and 0.817; the kappa values were 0.461, 0.681 and 0.690. It is concluded that differentiation between adenocarcinoma of the lung and malignant mesothelioma should be made on sections stained with H & E and mucin and/or immunohistochemical staining reactions, including antibodies against B72.3, Ber-EP4 and CEA.
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PMID:The histopathological diagnosis of malignant mesothelioma v. pulmonary adenocarcinoma: reproducibility of the histopathological diagnosis. 806 83

A relatively specific binding of lectins to various glycids enabled authors to evaluate the exosecretion characteristic of lung carcinomas closer than by HE, investigation of mucins and immunohistochemical epithelial markers. The main subtypes of lung adenocarcinomas (usual of acinar, tubulopillary cubocellular or cylindrocellular, solid with mucus production), pseudosarcoma, large cell and undifferentiated carcinomas from 9 bioptical samples were therefore compared as to binding of 5 lectins with preferential affinity to glucose/mannose (CON A), acetylglucosamin (WGA) and acetylgalactosamin (PNA, RCA, HPA). All the subtypes of adenocarcinoma as well as undifferentiated carcinoma showed a strong binding of bean lectin (CON A) and a slighter binding of ricinus (RCA) and wheat germ (WGA) lectins. Binding of Helix pomatia lectin (HPA) was nearly parallel to that of CON A even in large cell carcinoma (without mucin positivity)-except in undifferentiated carcinoma (in HE reminding of squamous carcinoma but CK negative). Peanut lectin (PNA) binding correlated with the production of acid glycosaminglycans and its lacking might serve as an indirect sign of Clara cell origin in some cubocellular bronchioloalveolar carcinomas which was otherwise difficult to prove. Lections mostly did not bind to mucus vacuoles and cytoplasmic granulary positivities represented secretion granules; marginal membranous positivities represented glycocalyx or lipoproteinaceous layer released by Clara cells in accordance with the expression of EMA. In pseudosarcoma a gradual binding of CON A from sarcomatoid to epithelial areas allowed to evaluate their connection better than according to an expression of cytokreatin.
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PMID:[Lectins in pulmonary adenocarcinomas]. 864 Aug 89

Many cell types of the salivary glands have clear cytoplasm. Causes of clear cytoplasmic quality in light microscopy are loss of organelles, storage of substances or fixation artefacts. Differential diagnosis of the different clear cell types requires special staining techniques, immunocytochemistry and electron microscopy. A new and distinct salivary gland neoplasm is hyalinizing clear cell carcinoma, which was not included in the second edition of the WHO Classification of Salivary Gland Tumors. Analysis of the collected cases of the Salivary Gland Register Hamburg and recent reports in the literature reveal that this carcinoma shows low-grade malignancy with localization usually in the minor salivary glands. Most cases occur in women. The pathohistology is characterized by solid or trabecular formations of polygonal clear cells which are surrounded by a broad hyalinized desmoplastic connective tissue stroma. The clear cells are mucin negative and express cytokeratin and EMA, in some cases also CEA, but not S-100 protein, actin or other markers of myoepithelial cells. Ultrastructural findings are undifferentiated duct cells with only few organelles and inclusion of glycogen granules. The differential diagnosis includes other clear cell tumours, especially epithelial-myoepithelial carcinoma and the clear cell variants of myoepithelial carcinoma and acinic cell or mucoepidermoid carcinoma.
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PMID:[Hyalinizing clear cell carcinoma of the salivary glands]. 865 Jan 36

Episialin (MUC1, PEM, EMA, CA15-3 antigen) is a sialylated, membrane-associated glycoprotein with an extended mucin-like ectodomain. This domain mainly consists of 30-90 homologous 20-amino acid repeats that are rich in O-glycosylation sites (serines and threonines). It is likely that this part forms a polyproline beta-turn helix. As a result, the ectodomain can protrude more than 200 nm above the cell surface, whereas most cell surface molecules do not exceed a length of 35 nm. Normally, episialin is present at the apical side of glandular epithelial cells. On carcinoma cells, however, it can be strongly overexpressed and it is often present over the entire cell surface. We have previously shown that episialin, if it is interspersed between adhesion molecules, nonspecifically reduces cell-cell and cell-extracellular matrix interactions in vitro and in vivo, presumably by steric hindrance caused by the extreme length and high density of the episialin molecules at the cell surface. To analyze the molecular mechanism for this anti-adhesion effect in more detail, we have now deleted an increasing number of repeats in the episialin cDNA and transfected the resulting mutants into murine L929 cells expressing the homophilic adhesion molecule E-cadherin. Here we show that the length of episialin is the dominant factor that determines the inhibition of E-cadherin-mediated cell-cell interactions. For the anti-adhesive effect mediated by the full length episialin, charge repulsion by negatively charged sialylated O-linked glycans is far less important.
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PMID:A mechanism for inhibition of E-cadherin-mediated cell-cell adhesion by the membrane-associated mucin episialin/MUC1. 873 Jan

We have encountered a series of 8 third ventricular neoplasms with a distinctive chordoid appearance that appear to represent a clinicopathologic entity. The tumors occurred in 7 females and 1 male, ranging in age from 31 to 70 years. In all cases, imaging studies showed a large well-circumscribed third ventricular mass; a cystic component was noted in 2. The tumors consisted of cords and clusters of cohesive, oval-to-polygonal epithelioid cells with abundant eosinophilic cytoplasm, relatively uniform round-to-oval nuclei, and inconspicuous nucleoli. Mitotic activity was absent. The stroma consisted of scant, coarse fibrillar processes, as well as prominent, slightly basophilic, extracellular mucin resembling that in chordomas. Throughout the tumor, and surrounding its well-defined borders, were infiltrates of mature lymphocytes and plasma cells. Russell bodies were prominent in the latter. Adjacent brain tissue showed reactive changes with gliosis and numerous Rosenthal fibers. Immunohistochemically, tumor cells were strongly reactive for GFAP and vimentin, but negative or only weakly staining for EMA. The MIB-1 labeling index was approximately 1%. Ultrastructural examination of 4 cases revealed focal microvilli, scattered "intermediate" junctions, and focal basal lamina formation. Neither desmosomes nor cilia were seen. Total resections were achieved in 2 cases; only subtotal removals were achieved in 6. Subsequent tumor enlargement was noted in 3 of the 6 patients with incomplete resection, and of these, two died at post-operative intervals of 8 months and 3 years. The other patient survives 4 years post-operatively with stable residual disease. Of the 2 patients with total resection, 1 was lost to follow-up; the other, during a brief follow-up period, did well without evidence of recurrence.
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PMID:Third ventricular chordoid glioma: a distinct clinicopathologic entity. 960 Feb 20


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