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)

Plasma protein adsorption is an important initial event in the response of tissue to foreign materials. Little is known about the way in which the chemical properties of materials influence the nature of the adsorbed layer and thus the later cellular responses. In this study, the amounts of fibrinogen, immunoglobulin G, albumin, and hemoglobin adsorbed from plasma to a series of HEMA-EMA random copolymers varying in hydrophilicity was measured. The adsorption of each protein varied in a characteristic way with copolymer composition probably reflecting a different affinity of the proteins for the various copolymers. A complex variation in the composition of the adsorbed protein layer on polymers varying in hydrophilicity was thus evident. Surface enrichment of the proteins, calculated as the ratio of the surface and bulk fraction of each protein, also varied with copolymer composition, and indicated substantial differences in the composition of the surface and bulk phases. Surface area variations among the copolymers, preferential adsorption of 125I proteins, and the possibility of structural degradation of 1,25I proteins in plasma were investigated but did not appear to influence the adsorption results. The ability of polymers to fractionate plasma proteins and concentrate them at their surface is concluded to be a key factor in the complex processes which determine the compatibility of polymers in vivo.
J Biomed Mater Res 1981 Sep
PMID:Adsorption of proteins from plasma to a series of hydrophilic-hydrophobic copolymers. II. Compositional analysis with the prelabeled protein technique. 1265 35

The etiology and pathogenesis of Hodgkin lymphoma (HL) are not yet known. There are implications of genes involved in programmed cell death (apoptosis), and there have been repeated suggestions of an association with Epstein-Barr virus (EBV). The aim of this study was to investigate the protein expression patterns of key cell cycle-related genes, together with evidence of apoptosis and EBV status, in relation to clinical stage in HLs. A double immunohistochemical and in situ hybridization technique was used to detect the expression of bcl-2, p53, retinoblastoma (Rb), p21, Ki67 (MIB 1), and topoisomerase IIalpha (TopoIIalpha), together with latent membrane protein-1 and EBER for EBV status and TdT-mediated dUTP-FITC nick end-labeling (TUNEL) as a measure of apoptosis, on tissue microarray sections of 62 cases of classic HL (35 NS, 17 MC, 8 LR, and 2 LD). A panel of phenotypic markers was used to facilitate recognition of Hodgkin and Reed-Sternberg (H-RS) cells: CD3, CD20, CD30, CD15, and EMA. The H-RS cells of 62 classic Hodgkin lymphomas were bcl-2-positive in 35 cases (56.45%), p53-positive in 14 (22.58%), and positive for both EBV latent membrane protein-1 and EBER in 37 (59.68%); there was complete concordance of results for EBV by both procedures. No correlation was found between expression of bcl-2, p53, or EBV markers in H-RS cells and clinical stage (P > 0.05). Expression of Rb, Ki67, p21, and TopoIIalpha did, however, show significant differences with clinical stage. Expression of Rb and p21 in CD30-positive H-RS cells decreased with more advanced stage (P < 0.001). In contrast, Ki67 and ToPoIIalpha expression increased with later stage (P < 0.01). No correlation was found between expression of any of these markers in H-RS cells and the subtypes of nodular sclerosis HL, mixed cellularity HL, and LRHL (P > 0.05). TUNEL was found in the nonneoplastic cellular background in all cases and in H-RS cells in only 10 of 62 cases (16.12%) (8 nodular sclerosis HL, 1 mixed cellularity HL, and 1 LRHL). There was a significant correlation between high expression of bcl-2 and a low score by TUNEL (P < 0.05). These data are consistent with the notion that overexpression of bcl-2 may be linked to blockage of apoptosis-mediated death of H-RS cells in classic HL. Abnormal expression of p53-related protein may not play a major role in HL, because it is present in H-RS cells in only a minority of cases. Increased expression of Ki67 and TopoIIalpha by H-RS cells is significantly associated with advanced stage and may indicate aggressive disease. Adverse clinical outcome in HL also is associated with loss of Rb and p21 protein expression, consistent with the possible roles of Rb and p21 in inhibition of the growth of H-RS cells. Within the limitations of the methods used, almost two thirds of cases of HL provide evidence of an association with EBV. The tissue microarray technique is valuable not only for examination of large numbers of cases of a disease by a complex panel of markers but also potentially as a control for staining quality in immunohistochemistry and in situ hybridization.
Appl Immunohistochem Mol Morphol 2003 Sep
PMID:Apoptosis and cell cycle-related genes and proteins in classical Hodgkin lymphoma: application of tissue microarray technique. 1296 46

Peripheral T-cell lymphoma (PTCL) is a group of diseases which are common in Asia and areas of South and Central America. They are highly associated with the Epstein-Barr virus (EBV) infection. In the present study the authors evaluated patients with gastrointestinal involvement of PTCL with respect to clinical findings and outcome, pathologic features, and molecular analysis for EBV infection and the clonality of tumor cells. From January 1997 through December 2000, 7 patients with gastrointestinal tract involvement of PTCL were identified. The frequency of gastrointestinal tract involvement in the various types of PTCL was 5.4 per cent (7 of 129 cases). The pertinent clinical features were prolonged fever, weight loss, anemia, hepatosplenomegaly, lymphadenopathy, multiorgan involvement, and gastrointestinal bleeding. Laboratory results showed a significantly high serum level of alkaline phosphatase and lactate dehydrogenase, and abnormal coagulograms. Five patients died within 4 months after onset of illness, while two were in complete remission after chemotherapy. The tumor cell morphology was classified into three categories: small-sized cells, mixed medium- and large-sized cells, and large-sized cells. The antigenic phenotypes of the tumor cells were LCA+, CD3+, CD15-, CD16-, CD30-, CD45R0+, CD57-, CD68-, EMA-, betaF1-, granzyme B+, TIA-1+, and p53+. The expression of CD4, CD8, CD56 and CD20 was variable. EBV-RNA expression by in situ hybridization (EBER-ISH) study was positive and T-cell receptor (TCR) beta and/or gamma gene rearrangements were detected in all patients. DNA sequence analysis showed high identity to the human TCR germline gene. PTCL with gastrointestinal tract involvement was associated with EBV infection. The tumor cells were mature T cells with some NK-cell antigenic expression and all demonstrated TCR gene rearrangements.
J Med Assoc Thai 2003 Sep
PMID:Epstein-Barr virus-associated peripheral T-cell lymphoma with gastrointestinal tract involvement. 1464 66

Based on clinical and histologic features, differentiating metastatic carcinomas from benign or malignant meningiomas usually is not difficult. Occasionally, however, in some patients without a clinical history of carcinoma, malignant meningiomas can morphologically simulate metastatic carcinoma, necessitating an immunohistochemical study for cytokeratin to make a correct diagnosis. However, the utility of immunohistochemical markers to separate malignant meningioma from metastatic carcinoma has not been investigated. The immunoperoxidase method with antigen retrieval was used to characterize the expression of three cytokeratins (AE1/AE3, CAM 5.2, and Pan cytokeratin), EMA, CEA, Ber-EP4, CD 15, and B72.3 in 12 previously diagnosed malignant meningiomas, 20 benign meningiomas, and 20 metastatic carcinomas. Cytokeratin expression was detected in 75% of malignant meningiomas, 0% of benign meningiomas, and 100% of metastatic carcinomas. While epithelial markers of Ber-EP4, CEA, B72.3 and CD-15 were positive in 90, 80, 70 and 65% of the metastatic carcinoma, respectively, they were negative in all 12 malignant meningioma examined. Vimentin immunoreactivity was seen in all benign and malignant meningiomas, and in 20% of metastatic carcinomas. Our results indicated that cytokeratin is not a reliable immunohistochemical marker to separate a malignant meningioma from metastatic carcinoma. A panel of epithelial markers including Ber-EP4, CEA, B72.3 and CD-15, and vimentin may be needed to separate malignant meningioma from metastatic carcinoma. Cytokeratin expression can be a potential pitfall for confusing a malignant meningioma with a metastatic carcinoma.
Mod Pathol 2004 Sep
PMID:Expression of cytokeratin by malignant meningiomas: diagnostic pitfall of cytokeratin to separate malignant meningiomas from metastatic carcinoma. 1513 78

Localizations of CEA,EMA and keration in 19 cases of mucoepidermal carcinomas were investigated using the indirect immunoperoxidase technique.The results showed CEA was negative in normal salivary glands and showed faint reaction in glands near carcinoma tissue.Keratin and EMA were localized in some myoepithelial cells.The positive rates in carcinoma tissue were 78.9%,89.5% and 84.2%,respectively.The positive rates and staining intensity of CEA and EMA in carcinoma tissue gradually decreased with the decline of tumor differentitation,but that of keratin showed no variation.the author consider that CEA and EMA could become good indices in clinically diagnosing mucoepithelial carcinoma and determining tumor differentiation type cell in mucoepidermal carcinoma and have a potential to multiply express the tumor elements of epithelium and/or mesenchyma.
Shanghai Kou Qiang Yi Xue 1993 Sep
PMID:[Immunohistochemical localization of CEA,EMA and keratin in salivary mucoepidermal carcinoma] 1515 29

Hypoxic stress induces apoptosis of hippocampal CA1 neurons while selectively sparing those in CA2-3. Proliferation and differentiation of local stem cells may potentially replace lost neurons. We examined MAP kinase signaling regulation of these dual responses. Rat organotypic hippocampal cultures were exposed to hypoxia for up to 6 h followed by reoxygenation. JNKs and ERKs were maximally activated by 4 h, returning approximately to basal levels by 6 h. Apoptosis of CA1 neurons was maximal by 6-h hypoxia, although JNK activation had returned to basal levels. A neuroprotective protein, JNK-interacting protein 1 (JIP1), an inhibitor of JNK-mediated apoptosis, was reduced by 6-h hypoxia and markedly decreased by 24-h reoxygenation in CA1 neurons as was DENN/MADD, which also modulates JNK-mediated cell death. A second peak of ERK1 activation occurred at 24-h reoxygenation and declined to control levels by 48 h. Stem cells were detected by antinestin and cell proliferation confirmed with anti-PCNA immunohistochemistry and BrdU incorporation. With U0126, an inhibitor of ERK activation, BrdU labeling was strikingly reduced implicating ERKs in the proliferation response. Antidoublecortin (DCX), which detects neural progenitor cells, colabeled a subset of BrdU-positive cells that extended from the dentate granule neurons into CA1. Astrocytes were colabeled with BrdU. Thus, hypoxia concurrently triggered both JNK and ERK signaling, and with reoxygenation, ERK1 activation and stem cell proliferation followed by neuronal progenitor cell differentiation and targeted migration to the site of pyramidal neuronal loss.
Brain Res 2004 Sep 17
PMID:Neurogenesis response to hypoxia-induced cell death: map kinase signal transduction mechanisms. 1532 27

The case of a soft tissue myoepithelioma is presented including clinicopathologic, ultrastructural, and genetic findings. A 30-year-old male patient suffered from a soft tissue tumor within the deep soft tissues of the right lower leg measuring 13.2 x 8.2 x 9 cm. Histologically, the lesion was diagnosed as a myoepithelioma displaying a lobulated architecture with cords and nests of epithelioid and spindle cells without cytologic atypia lying within a fibromyxoid and partly chondroid matrix; immunohistochemistry was positive for pancytokeratin, S100-protein, calponin and partly for GFAP and EMA. Ultrastructural analysis revealed glycogen deposits and cell-membrane-associated plaque structures, whereas true myofilaments could not be identified (with immunohistochemistry being negative for actin). Using comparative genomic hybridization (CGH), a gain of chromosome Y was detected. A loss on 17p could not be detected unambiguously. However, based on the low resolution of CGH a small loss cannot be excluded. The patient was free of disease 25 months following complete tumor resection. Myoepitheliomas/mixed tumors of deep soft tissue represent rare soft tissue lesions that may reach a considerable size and may mimic other soft tissue tumors or sarcomas. Based on a local relapse rate of approximately 20% according to the literature, a complete resection with thorough follow-up should be recommended.
Pathologe 2005 Sep
PMID:[Myoepithelioma of soft tissue -- case report with clinicopathologic, ultrastructural, and cytogenetic findings]. 1603 88

Sarcomatoid carcinomas are uncommon, high-grade tumors, predominantly composed of spindle cells. Only a few cases arising in the penis have been reported. The aim of this study is to better define the clinicopathologic features of this neoplasm. A total of 400 cases of squamous cell carcinoma of the penis were reviewed from which 15 sarcomatoid carcinomas (4%) were identified. Clinical and pathologic features were evaluated in all cases. Immunohistochemical studies for expression of AE1/AE3, Cam 5.2, 34betaE12, EMA, vimentin, muscle specific actin, smooth muscle actin, desmin, S-100, p63, and p53 and in situ hybridization studies for HPV were performed in 5 cases. Information about lymph node status was available in 9 cases, and follow-up in 5 cases. The mean age was 59 years, and mean tumor size was 5 cm. Grossly, most tumors were large, polypoid, and ulcerated masses frequently affecting the glans (93%) and deeply invading corpora cavernosa (80%) and skin. Microscopically, the lesions were predominantly composed of atypical spindle cells disposed in interlacing fascicles, resembling fibrosarcoma or leiomyosarcoma, sometimes admixed with pleomorphic giant cells mimicking malignant fibrous histiocytoma. One case was predominantly composed of myxoid areas. Less frequent and focal patterns were pseudoangiomatous and epithelioid. Mitotic figures were numerous, and necrosis was prominent. Foci of heterologous differentiation toward bone (osteosarcomatous component) were present in 1 case. Four cases showed a minor mixed component of usual, papillary, verrucous, and basaloid carcinoma. Intrapenile metastasis ("satellitosis") was present in 4 tumors. One of the cases was multicentric with a separate independent focus of well-differentiated carcinoma with pseudohyperplastic features. Associated low- and high-grade squamous intraepithelial lesions were noted in 73% of the cases. Immunohistochemical studies and HPV in situ hybridization were done in 5 cases. The spindle cells were diffusely positive for vimentin and p53 and showed at least intermediate expression of 34betaE12 and p63 in all cases. EMA and AE1/AE3 were focally positive in 60% of the cases, and Cam 5.2 was focally positive in 1 case. Tumor cells failed to express muscle specific actin, smooth muscle actin, desmin, and S-100. HPV in situ hybridization was negative in all cases. Inguinal metastases were present in 89% of the cases. Two of five patients with adequate follow-up died of disease within 8 months of the diagnoses. In conclusion, penile sarcomatoid carcinomas are unusual, large, and aggressive tumors usually associated with lymph node metastasis and poor outcome. Differential diagnoses include sarcoma and melanoma. Cytokeratin 34betaE12 and p63 appear to be the more specific and sensitive markers to categorize these tumors as epithelial. Diffuse immunoreactivity for p53, compared with a more basal and focal reactivity in differentiated squamous cell carcinoma, may be indicative of a late mutation in the natural progression of the disease.
Am J Surg Pathol 2005 Sep
PMID:Sarcomatoid carcinoma of the penis: a clinicopathologic study of 15 cases. 1609 3

Only two karyotypes of perineurioma have previously been reported, 46XX,del(10)(q22q24),der(10),del(22)(q11-12q?)/47, idem,+der(10) (in a sclerosing perineurioma of the finger) and 45,XX,add(14)(p13),-22,add(22)(q11.2) (in an intraneural perineurioma). We investigated the clinicopathologic and cytogenetic findings in four consecutive perineuriomas in children, including two small (< or =1 cm) digital sclerosing perineuriomas, a 2-cm intraneural perineurioma, and a 16-cm abdominal soft tissue perineurioma. All lesions showed plump perineurial cells in a complex whorled configuration. Immunohistochemical (strong EMA immunostaining in all cases) and ultrastructural (in three of three lesions examined) evidence of perineurial differentiation was present. The sclerosing perineuriomas showed 46,XY,t(2;10)(p23;q24) and 47,XX,add(3)(q23),add(6)(q21),-5,-9,-10,-22,+mar1,+mar2,+mars; the intraneural tumor showed 46,XX,add(2)(q11.2),add(3)(q12); and the abdominal soft tissue perineurioma showed 46,XX,t(8;9)(q13;q22). Metaphase FISH analysis for an ALK gene rearrangement in the sclerosing perineurioma with t(2;10) was negative; the ALK signal remained on the der(2). We conclude that perineuriomas display mostly simple karyotypes, characterized by one or few chromosomal rearrangements or numerical changes. In conjunction with the previously published sclerosing perineurioma karyotypes, the findings of chromosome 10 aberrations, t(2;10)(p23;q24) and monosomy 10 in two sclerosing perineuriomas, indicate that rearrangements and/or deletions of 10q are a consistent finding in this variant of perineurioma. The findings also expand previous assertions that chromosome 22 abnormalities are pathogenetic in perineurioma and suggest that diverse genetic tumorigenic mechanisms may exist, possibly depending on the subtype.
Am J Surg Pathol 2005 Sep
PMID:Cytogenetic aberrations in perineurioma: variation with subtype. 1609 5

A novel human mammary epithelial cell line, HME348, was established from benign breast tissue from a 44-year-old germ-line BRCA2 mutation carrier with a history of stage 1 breast cancer. Mutation analysis showed that the patient had a known 6872del4 BRCA2 heterozygous mutation. The human mammary epithelial cells passaged in culture exhibited cellular replicative aging as evidenced by telomere shortening, lack of telomerase activity, and senescence. Ectopic expression of telomerase (hTERT) reconstituted telomerase activity in these cells and led to the immortalization of the cells. When grown on glass, the majority of immortalized HME348 cells expressed ESA and p63 with a small population also expressing EMA. In three-dimensional Matrigel culture, HME348 cells formed complex branching acini structures that expressed luminal (EMA, CK18) and myoepithelial (p63, CALLA, CK14) markers. Three clones derived from this culture were also p63(+)/ESA(+)/EMA(+/-) on glass but formed similar acinar structures with both luminal and myoepithelial cell differentiation in Matrigel confirming the mammary progenitor nature of these cells. Additionally, the experimentally immortalized HME348 cells formed acini in cleared mammary fat pads in vivo. As this is the first report establishing and characterizing a benign human mammary epithelial cell line derived from a BRCA2 patient without the use of viral oncogenes, these cells may be useful for the study of BRCA2 function in breast morphogenesis and carcinogenesis.
Breast Cancer Res Treat 2006 Sep
PMID:Telomerase immortalization of human mammary epithelial cells derived from a BRCA2 mutation carrier. 1654 10


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