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)

In this study, a clinicopathologically and immunophenotypically diverse group of T-cell neoplasms were evaluated by one- and two-color flow cytometry and/or immunohistochemistry for the presence of eight antigens (T10, T9, IL2-R, EMA, HLA-DR, LeuM1, Ki-1, and LeuM5) which are expressed in a hierarchical manner by phytohemagglutinin (PHA)-activated benign T cells. We found that 70 of the 72 T-cell neoplasms (97%) expressed at least one of these eight T-cell activation-associated antigens (T-AAgs) and that the number and type of T-AAgs expressed by the neoplastic T cells varied according to the clinicopathologic category of T-cell neoplasia. All 5 T-cell lymphoblastic malignancies expressed T10 and T9; 2 also expressed LeuM1. Twelve of 14 (86%) T cell chronic lymphocytic leukemias (T-CLL) expressed two to four T-AAgs, most frequently T10 (86%) and HLA-DR (79%). The 26 cutaneous T-cell lymphomas (CTCL) expressed between 2 and 5 T-AAgs, most commonly T9 (92%) and HLA-DR (92%), and least often T10 (12%) and EMA (15%). Twenty-six of 27 (96%) peripheral T-cell lymphomas (PTCL) expressed more than 4 T-AAgs. Each of the T-AAgs were expressed by between 22% (LeuM5) and 85% (T9) of the PTCLs. Some T-AAgs were preferentially expressed by the PTCLs in association with other T-AAgs, such as EMA in association with IL2-R and Ki-1. In addition, LeuM5 was preferentially expressed by CD4- CD8+ T-cell neoplasms. However, only 19 of the 72 (26%) T-cell neoplasms (3/5 lymphoblastic malignancies, 3/14 CLLs, 0/26 CTCLs, 13/27 PTCLs) expressed T-AAg immunophenotypic profiles paralleling those expressed by normal peripheral blood T cells activated in vitro with PHA. These results suggest that T-AAg expression by neoplastic T cells does not often mirror the hierarchical order of expression by activated benign T cells, implying that neoplastic T cells do not usually represent the precise malignant counterpart of activated benign, normal T cells.
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PMID:T-cell activation-associated antigen expression by neoplastic T-cells. 142 41

CD30/Ki-1 antigen expression in 243 cases of malignant lymphomas was examined using Ber-H2 monoclonal antibody. Among them 20 cases were categorized as Ki-1 anaplastic large cell lymphoma. In two of these cases histiocyte-associated markers were also expressed. In these cases histopathologic and extensive in situ immunophenotypic analyses were used with genotypic studies in the determination of cell lineage. A sinusoid histologic pattern of involvement with partial lymph node infiltration by pleomorphic neoplastic cells was noticed in the nodes from both patients. Solid areas of node replacement resembling metastatic carcinoma were seen in Patient 1. Immunohistologically, tumor cells of both cases were positive for CD30, CD25, CD71, LN3 (HLA-DR), EMA, CD45, CD74, vimentin, alpha-1-antichymotrypsin, and CD68. Patient 1 was also CD45RO+, CD43+, whereas Patient 2 was positive for alpha-1-antitrypsin and CD4 tumor cells. Genotypic studies revealed that TCR beta and TCR gamma chain genes were clonally rearranged in Patient 1, whereas no rearrangements were detected in Patient 2. This study supports the view that some Ki-1 anaplastic large cell lymphomas may express multiple histiocyte-associated antigens and confirms that this group of neoplasms have immunophenotypic heterogeneity. The results of genotypic analyses used with immunophenotyping does not exclude that the tumor cells in these cases may be of true histiocytic origin despite the Ki-1-positive phenotype.
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PMID:Histopathologic, immunophenotypic, and genotypic analysis of Ki-1 anaplastic large cell lymphomas that express histiocyte-associated antigens. 217 1

A case of lymphocyte-depletion Hodgkin's disease is described for the purpose of reviewing the criteria currently used to distinguish this disease from other pleomorphic large-cell malignancies. A 76-year-old man with a 3-month history of daily fevers underwent extensive evaluation and exploratory laparotomy, which revealed only two large, separate splenic tumor nodules. Postoperatively, the patient remained asymptomatic. Histologically, the tumor was composed of giant cells, including both typical Reed-Sternberg forms and mononuclear variants with inflammatory stromal response along its borders. Immunoperoxidase showed tumor cells to be strongly reactive for Leu-M1 (CD15), BER-H2 (CD30), Leu-3 (CD4), and T11 (CD2) and weakly reactive for Leu-4 (CD3) but nonreactive for EMA, LCA, lysozyme, Leu-9, Leu-M3, Leu-M5, and immunoglobulin light chains. Southern blot analysis revealed an isolated clonal band for kappa light chain only. Included in the discussion of this case of primary splenic lymphocyte-depletion Hodgkin's disease is a review of clinical, histologic, immunohistochemical, and gene-rearrangement characteristics of what can be defined as lymphocyte-depletion Hodgkin's disease.
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PMID:Primary splenic lymphocyte-depletion Hodgkin's disease. 222 Jun 73

A laparotomy performed for an occlusive syndrome, disclosed the presence of an ileal lymphoma in a renal graft recipient, 17 years after a first renal transplant. Mesenteric lymph node and spleen involvement were associated. The morphology of the large cells, the type of infiltration of the lymph node simulating metastatic carcinoma or malignant histiocytosis were highly suggestive of a new type of high grade malignancy lymphoma recently described which is called 'large cell anaplastic ML'. The immunolabelling study confirmed this diagnosis, demonstrating the following phenotype CD4, CD25 (TAC), CD30 (Ki-1), OKT 9 (transferrin receptor), EMA and HLA DR positivity. The tumour cells were negative for the other T, B and histiomonocytic markers. This case, of a large cell anaplastic Ki-1 positive lymphoma, expressing CD4, in a renal graft recipient shows that high grade ML in such patients are not all of the B cell type.
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PMID:Primary intestinal lymphoma of Ki-1 large cell anaplastic type with mesenteric lymph node and spleen involvement in a renal transplant recipient. 255 76

We studied the reactivity of malignant mesothelioma cells with tumor markers and the phenotypes of lymphocyte subsets in pleural effusions from 14 patients with malignant mesothelioma. For identification of cell surface antigens with monoclonal antibodies, the adhesive slide assay was used. The reaction pattern of mesothelioma cells was found to be CEA negative, Leu M1 negative, EMA positive, BMA-120 positive, My 4 positive, and BA-2 positive. The surface morphology of mesothelioma cells may be of additional help for diagnosis. By these markers, the distinction between mesotheliomas and carcinomas is facilitated. The differentiation of reactive benign mesothelial hyperplasia from malignant mesothelioma by surface marker staining is not yet possible, however. In many effusions in this study, a concomitant T-lymphocytosis was observed with a non-specific increase in the CD4/CD8 ratio, as known for other pleural diseases.
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PMID:Immunocytology in malignant pleural mesothelioma. Expression of tumor markers and distribution of lymphocyte subsets. 264 76

Immunohistochemical techniques were used to study the presence of cyclosporin A (CsA) and leukocyte subsets in 30 gingival biopsies of renal transplant subjects with gingival overgrowth (GO). Statistical analysis revealed significant differences in the total number of inflammatory cells determined by monoclonal antibody CD45, the monocyte/macrophage (CD68) subset, the plasmatic cells (EMA), and the total of T-lymphocytes (CD3) (P < 0.001, Student t test) between the treated subjects and the healthy control group. Differences were found in the helper/inducer T lymphocytes CD4 (P < 0.001 Student t test) and cytotoxic/suppressor T lymphocyte (CD8) (P < 0.01, Student t test) subsets between both groups. The CD4/CD8 ratio was greater in the transplant subjects than in the control group (1.82 +/- 0.16 versus 1.35 +/- 0.05 respectively) (P < 0.05 Student t test). There was no significant difference in the populations CD16+, CD57+, and CD20+. The CD45+ CD4+, and CD68+ cells increased in number along with the degree of GO. The number of epithelial cells/mm2 which displayed a deposit of CsA increased in accordance with the degree of GO (P < 0.05, Kruskal-Wallis's test). Likewise, the intraepithelial deposit of CsA in the GO region was found to be related to the inflammatory infiltrate CD4+, CD8+, and CD68+ (r = 0.7432; r = 0.7346; r = 0.77005, respectively). Our findings suggest that the intraepithelial deposit of CsA and the inflammatory infiltrate play a predominantly pathogenic role and are both related to the degree of GO.
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PMID:Immunohistochemical study of 30 cases of cyclosporin A-induced gingival overgrowth. 760 52

Non-Hodgkin's lymphomas uncommonly present as bone lesions. Most of these tumors are diffuse large B-cell lymphomas. Anaplastic large cell lymphoma (ALCL) presented as bone lesions is exceedingly rare. In this study, we describe six cases of ALCL that presented as solitary or multiple bone lesions. The average patient age was 33 years (range, 4 to 63 years) and the male to female ratio was 2:1. Fever and localized bone pain were the most frequent presenting symptoms. Radiologic examinations revealed osteolytic lesions in all cases, with three (50%) being multiple lesions and five (83%) involving the axial bones. All patients were initially assessed to have only bone involvement. Staging studies revealed mild cervical lymphadenopathy in one patient and no evidence of extraskeletal disease in the other five patients. Histologically, there was diffuse infiltration of one or more bones by large pleomorphic lymphoma cells. Immunohistochemical studies showed all six neoplasms were positive for CD30, EMA, and granzyme B. One case was of T-cell lineage, positive for CD3. One case was positive for the T-cell-associated antigen CD4. The remaining four cases were of null-cell type. In-situ hybridization for EBV was performed in five cases; all were negative. Despite the relatively low International Prognostic Index (IPI) of these patients (mean, 1.67; range, 1 to 3), the overall prognosis was relatively poor: three of six died of disease within 2 years of diagnosis, and two of six were alive with evidence of disease (follow-up, 6 mo to 2 years). Thus, compared to their nodal counterparts, ALCLs that present as bone lesions are distinguished by their uniform expression of EMA and granzyme B, and a relatively poor clinical outcome. Our results also suggest that ALK-1 expression in this clinical setting is not a favorable prognostic indicator.
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PMID:Anaplastic large cell lymphomas presented as bone lesions: a clinicopathologic study of six cases and review of the literature. 1104 10

A case of primary gastric T-cell lymphoma, which was positive for granzyme B, is reported. The patient was a 47-year-old Japanese female who complained of a dull upper abdominal pain. Radiographic and endoscopic examinations revealed an ulcerative infiltrative lesion in her stomach. Following the confirmation of a high-grade malignant lymphoma, a distal gastrectomy with regional lymph nodal dissection was performed. The histology of the gastric lesion revealed a malignant lymphoma of the diffuse pleomorphic type without lymph nodal involvement. Immunohistochemistry revealed that the tumor cells were positive for LCA, CD3, TIA-1 and granzyme B, but were negative for CD4, CD8, CD56, CD30, L-26, EMA, TCR alpha/beta and TCR gamma/delta. Because the tumor cells showed T cell nature with cytotoxic activity proved by TIA-1 and granzyme B, and without evidence of further maturation of T cell, a malignant lymphoma originating from extrathymic-derived T cells was suggested.
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PMID:Granzyme B-positive primary gastric T-cell lymphoma: gastric T-cell lymphoma with the possibility of extrathymic T cell origin. 1110 59

A study commissioned by the Philadelphia EMA HIV Commission shows that many people have a poor understanding about HIV transmission and treatment. The survey of 1,069 people found that lack of knowledge of HIV was greater among African-Americans and Latinos, who were also less likely to know their CD4 counts or viral load, and who were less likely to use combination treatments. Many HIV-positive people do not comprehend the need to start medical treatment early. The commission advises the Philadelphia Health Department to disperse more HIV treatment information among communities of color.
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PMID:Study finds poor knowledge about HIV. 1136 36

We describe a patient with leukopenic T-cell chronic lymphocytic leukemia/prolymphocytic leukemia (T-CLL/PLL), according to the Revised European-American Classification of Lymphoid Neoplasms. This patient simultaneously developed classic Hodgkin's disease (HD), a combination previously unreported. The leukemic cells were small and mature, did not have cytoplasmic granulation, and appeared similar to B-cell chronic lymphocytic leukemia. Immunophenotyping of the bone marrow-infiltrating cells revealed a postthymic suppressor/cytotoxic phenotype of CD2+, CD3+, CD4, CD5+, CD8+, CD25-, TCR-alpha beta. A lymph node biopsy showed the histological features of HD (mixed cellularity) with infiltrating CD8+ lymphocytes, and immunohistochemical examination revealed the following phenotype of Reed-Sternberg cells: LeuM1/CD15+, BerH2/CD30+, L26/PanB-, UCHL-1/CD45RO-, cyCD3-, CD4, CD8-, CD20-, CD79a-, EMA-, EBER-1+, LMP-1+. Southern blot analysis of the bone marrow and lymph node revealed the same rearrangement of bands of T-cell-receptor genes. Although the HD was treated with chemotherapy that resulted in complete remission, the T-PLL/CLL took an indolent course. This case may suggest the existence of a subtype of T-CLL/PLL with leukopenia and an indolent clinical course. Both diseases were believed to be independent and not a transformation of one to the other.
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PMID:Concurrent Hodgkin's disease (mixed cellularity type) and T-cell chronic lymphocytic leukemia/prolymphocytic leukemia. 1137 37


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