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)

Using indirect immunofluorescence and a panel of human convalescent-phase sera, we identified cytomegalovirus (CMV) early and late membrane antigens (CMV-EMA and CMV-LMA, respectively) as separate entities on the surfaces of viable CMV-infected fibroblasts starting at 6 to 12 and 36 to 48 h postinoculation, respectively. For expression of CMV-EMA and CMV-LMA, infectious virus and active protein synthesis were required, whereas the expression of CMV-LMA, in addition, required viral DNA synthesis. Our data suggest that CMV-EMA and CMV-LMA form an individual set of CMV antigens that are different from intracellular CMV antigens and possibly (partly) different from the viral envelope.
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PMID:Cytomegalovirus early and late membrane antigens detected by antibodies in human convalescent sera. 298 17

We report a rare gastric tumour characterized morphologically by its hepatoid features and alpha-fetoprotein production and which presented clinically with gastric haemorrhage. Gastric fibroscopy showed a bleeding tumour of the antrum. The microscopic appearance of the tumor showed two different patterns. The most extensive presented hepatoid features. The second pattern showed undifferentiated features. The tumour cells showed immunohistochemical positivity for alphafetoprotein, EMA and p53 protein; 37% were aneuploid with a DNA index of 1.46. The serum level of alphafetoprotein was not measured before the gastrectomy but after ten days it was elevated at 1070 ng/ml. The patient died 6 months after the admission. This case provides, for the first time, information on the DNA content and the p53 expression of this unusual and aggressive variant of gastric adenocarcinoma.
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PMID:Alphafetoprotein-producing gastric adenocarcinoma. 753 18

We have recorded 8 patients presenting a Hodgkin's disease associated with Castleman's disease. Four men and 4 women with a 44 years mean age (15-60), presented as a solitary mass (2/7) or as a multicentric tumoral disease (5/7). One of our patients was HIV. Histological studies showed typical features of Castleman's disease. Nodular sclerosing Hodgkin's disease with numerous lacunar cells were present in 3 cases, interfollicular Hodgkin's disease in 4 cases and nodular paragranuloma in one case. Hodgkins' and Reed Sternberg cells were positive for CD15 (4/7), CD30 (5/7), EMA (3/6) and LMP-1 (4/5). In situ hybridization on tissue sections demonstrate presence of EBV DNA in one case and EBER1-RNA in 2 of 4 cases. The difficulty in making the diagnosis of Hodgkin's disease the relation between both diseases, and the role of IL-6 are discussed.
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PMID:[Association of Castleman's disease and Hodgkin's disease. Eight cases and review of the literature]. 785 13

An 82-year-old male presented with a two-month history of hoarseness. A 2 cm pedunculated lesion was removed from the base of his epiglottis. Microscopy showed a polypoid atypical spindle cell lesion. Multiple levels failed to reveal an invasive squamous cell carcinoma. On the basis of haematoxylin and eosin stained sections the main differential diagnosis was a pseudosarcoma with an overlying dysplastic squamous mucosa or infiltrating spindle cell carcinoma. Immunohistochemistry showed positive staining for vimentin but no convincing staining with antibodies to cytokeratin and EMA. Ultrastructural analysis also failed to reveal epithelial characteristics. Ploidy analysis by static cytophotometry of the spindle cell proliferation revealed an aneuploid stem line with a DNA index of 1.67. On the basis of this the process was felt unlikely to be reactive and a diagnosis of a spindle cell squamous carcinoma was made. This diagnosis was subsequently supported by a clinical recurrence of the nodule at a six-month follow-up.
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PMID:Pseudosarcoma of the larynx: the value of ploidy analysis. 802 62

Seven cases of PCNP were studied; 5 females and 2 males, ages ranging from 21 to 68 years (mean 39). All had asymptomatic masses located in the head (3), body (2), isthmus (1) and tail (1). In 4 of them fine-needle aspiration (FNA) was done and showed a diagnostic pattern with papillary clusters as well as isolated epithelial cells with monomorphic appearance, round nuclei and inconspicuous nucleoli; 5 cases had a surgical resection and only 2 a biopsy due to unresectable tumors. Histologically, they showed the typical features of PCNP with solid, papillary, trabecular and cystic patterns. IHQ studies showed positivity for cytokeratin (n = 5), alpha-1-antitrypsin (n = 4), monoclonal NSE (n = 3), chromogranin (n = 3) and estrogen receptors (n = 1). All cases were negative for insulin, glucagon, somatostatin, EMA and CEA. DNA analysis done with an image analyzer showed 4 diploid tumors, 2 diploid-tetraploid an 1 aneuploid tumor. One patient died because of postoperative complications and the remaining 6 are alive with a mean follow-up of 17 months (2-36). We emphasize the diagnostic appearance of the tumor on FNA, and the low grade malignant potential of this neoplasm supported by the predominance of diploid tumors. Our IHQ findings suggest both an exocrine and endocrine differentiation.
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PMID:[Papillary and cystic tumors of the pancreas. Clinico-pathological, cytopathological, immunohistochemical, and nuclear ploidy study]. 808 43

In this study, we examine 10 primary carcinomas of Bartholin's gland, including seven squamous carcinomas, two adenoid cystic carcinomas, and one adenocarcinoma, as well as four non-neoplastic Bartholin's gland. Six of seven squamous cell carcinomas contained human papillomavirus (HPV) type 16 DNA detectable by the polymerase chain reaction; one of these demonstrated HPV type 16 by in situ hybridization. The two adenoid cystic carcinomas, the adenocarcinoma, and the non-neoplastic Bartholin's gland epithelium showed no evidence of HPV DNA by polymerase chain reaction or in situ hybridization. A panel of eight antibodies (Cam 5.2, B72.3, CEA, EMA, MCA, Lewis X, ER, and PR) demonstrate that the squamous, transition zone, duct, acinar, and myoepithelial cells or Bartholin's gland are antigenically distinct, and are similar to those reported in analogous areas of the uterine cervix. Squamous carcinoma and adenocarcinomas of Bartholin's gland are antigenically similar, and seem to arise from the transition zone of the Bartholin's gland duct. The origin of adenoid cystic carcinomas is more difficult to determine; it is distinct from squamous and adenocarcinomas and seems more likely to arise from myoepithelial cells. We conclude that adenocarcinoma and squamous cell carcinoma of Bartholin's gland arise in the transition zone of Bartholin's gland, which is similar to the transition zone of the uterine cervix. We also show that HPV is associated with Bartholin's gland carcinoma and may play a role in the genesis of malignancy.
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PMID:Carcinomas of Bartholin's gland. Histogenesis and the etiological role of human papillomavirus. 838 9

A case of parachordoma in a 45-year-old female was described. Histologically, the recurrent lesion, in comparison with the primary tumor, demonstrated an increased cellular atypia and mitotic rate. The tumor cells expressed EMA, vimentin, S 100 protein, and also a trace desmin content was present. Electron microscopic study provided no characteristic features of the tumor type studied. Flow cytometric evaluation of the DNA demonstrated a diploid histogram with the relatively high S-phase. Cytogenetic analysis revealed normal karyotype, but a deviation from the diploid state in the form of aneuploid metaphases with non-clonal structural chromosomal aberrations was observed.
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PMID:Parachordoma--a clinicopathologic, immunohistochemical, electron microscopic, flow cytometric, and cytogenetic study. 854 7

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

Several lines of investigation point to a new herpesvirus, human herpesvirus-8 (HHV-8), as the cause of two different neoplasms seen in AIDS patients-Kaposi's sarcoma (KS) and body cavity B cell lymphoma. If this virus is the etiological agent, rather than another opportunistic infectious agent, it should be present in the earliest detectable clinical lesions on a temporal basis, and localize to specific target cells in a spatial pattern consistent with tumorigenic pathways. In this study, we take advantage of the clinical accessibility to biopsy early (patch stage) skin lesions of KS to address the temporal issue, combined with in situ PCR and dual immunostaining using a marker identifying malignant cells, to address the spatial localization issue. 21 different tissue samples were subjected to PCR analysis and in situ PCR with and without simultaneous immunostaining. In normal skin from healthy individuals, no HHV-8 DNA was detected by PCR or in situ PCR. However, in all PCR-positive tissues, distinct and specific in situ PCR staining was observed. In four different patch stage KS lesions, in situ PCR staining localized to nuclei of endothelial cells and perivascular spindle-shaped tumor cells. Later stage KS lesions (plaques and nodules) revealed additional positive cells, including epidermal keratinocytes (four of five), and eccrine epithelia (two of four). These patterns were nonrestricted to skin, as pulmonary KS also revealed HHV-8-specific infection of endothelial cells and KS tumor cells, as well as epithelioid pneumocytes (two of two). In body cavity B cell lymphoma by dual staining, HHV-8 was present in malignant tumor cells (EMA immunostained positive) and not in reactive lymphocytes. These results reveal an early temporal onset and nonrandom tissue and cellular distribution pattern for HHV-8 infection that is consistent with a causal link between this DNA virus and two AIDS-related neoplasms.
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PMID:In situ polymerase chain reaction-based localization studies support role of human herpesvirus-8 as the cause of two AIDS-related neoplasms: Kaposi's sarcoma and body cavity lymphoma. 918 21

Long-chain acyl-CoA dehydrogenase (LCAD) is one of four enzymes involved in the initial step of mitochondrial beta-oxidation of straight-chain fatty acids. It is a member of the acyl-CoA dehydrogenase (Acad or ACAD) gene family of enzymes, which also includes very-long-chain (VLCAD), medium-chain (MCAD), and short-chain (SCAD) acyl-CoA dehydrogenases. These enzymes all have similar activity but differ only in the chain length specificity for their substrate. Mitochondrial beta-oxidation provides an important source of energy especially during times of fasting. In order to understand the role of LCAD in this pathway, we have cloned and characterized the entire mouse (Mus musculus) gene encoding LCAD (Acadl). Acadl is a single-copy, nuclear encoded gene approximately 35 kb in size. We have sequenced the entire coding region, all intron/exon boundaries, 1.7 kb of its 5' regulatory region, and mapped the transcription start site. The gene contains 11 coding exons ranging in size from 67 bp to 275 bp, interrupted by 10 introns ranging in size from 1.0 kb to 6.6 kb in size. The Acadl 5' regulatory region, like other members of the Acad family, lacks a TATA or CAAT box and is GC rich. This region does contain multiple, putative cis-acting DNA elements recognized by either SP1 or members of the steroid-thyroid family of nuclear receptors, which has been shown with other members of the ACAD gene family to be important in regulated expression. The characterization of the mouse Acadl gene will allow further study of LCAD in an in vivo model, and how its expression may be coordinated with other members of the Acad gene family.
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PMID:Structural characterization of the mouse long-chain acyl-CoA dehydrogenase gene and 5' regulatory region. 954 92


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