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Query: UMLS:C0268596 (EMA)
 2,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Both immunophenotypic overlaps between Hodgkin's disease (HD) and non-Hodgkin's lymphoma (NHL), and evolution of one into the other have been reported. However, the underlying assumption that the antigenic expression of Reed-Sternberg (RS) cells is consistent in the same patient has not been evaluated. Such an evaluation was undertaken by immunophenotyping paraffin-embedded lymphoid tissue biopsies with HD from 56 patients in whom multiple specimens were obtained, either simultaneously from different sites or at different times. The panel of antibodies we used included: CD3 polyclonal antiserum, DAKO-M1 (CD15), L26 (CD20), BerH2 (CD30), MT1 (CD43), DAKO-LCA (CD45RB), UCHL1 (CD45R0), LN2 (CD74), and DAKO-EMA. The phenotype of RS cells was identical in simultaneous biopsies in only 11 of 39 patients (28%) and remained constant in consecutive biopsies in only 4 of 21 patients (19%). Major differences (relative to cell lineage specific antigens) were observed in 10 of 39 patients with simultaneous biopsies and in 10 of 21 patients over time; they mainly involved expression of T-cell antigens. Minor differences (relative to any other antigen) were observed in 22 of 39 patients with simultaneous biopsies and in 15 of 21 patients over time; these mainly involved CD15 or CD74. This striking variability of the immunophenotype of RS cells in the same patient may be due to aberrant marker expression, as a result of the neoplastic state, and/or to modulation of antigenic expression in relation to the host environment. This inconsistency suggests caution when interpreting the relationship between HD and NHL by paraffin immunophenotyping alone.
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PMID:Inconsistency of the immunophenotype of Reed-Sternberg cells in simultaneous and consecutive specimens from the same patients. A paraffin section evaluation in 56 patients. 135 42

Epstein-Barr virus (EBV) has been demonstrated in the Reed-Sternberg cells and their mononuclear variants (Hodgkin cells; H-RS cells) in a substantial number of Hodgkin's disease (HD) cases. Moreover, EBV can modulate both in vivo and in vitro the expression of several cellular genes, including lymphoid differentiation markers. Therefore we investigated, in 64 cases of HD, the relationship between the presence of EBV and the expression of lymphoid (CD45RB), T- (CD3, CD45RO), B- (CD20, MB2 antigen, CDw75), and myeloid-cell lineage markers (CD15), and of activation markers (CD30, EMA, and the 115D8 antigen) on the H-RS cells. EBV-positive cases, as demonstrated by the presence of EBER-1 and -2 RNA and LMP-1 protein expression, showed a significant reduction in the expression on H-RS cells of T-cell lineage (CD3, P < 0.02), B-cell lineage (CD20; P < 0.005), and activation markers (EMA; P < 0.002 and the 115D8 antigen; P < 0.001) as compared with EBV-negative cases. No differences were found in the expression of CD15, CD30, CD45RO, CD45RB, CDw75, or the MB2 antigen on H-RS cells in EBV-positive and EBV-negative HD cases. Interestingly, in 11 cases of EBV-negative HD, B- as well as T-cell lineage markers could be found on some H-RS cells. These data suggest that EBV in H-RS cells is able to down-regulate the expression of T- (CD3) and B- (CD20) cell lineage markers and lymphoid activation markers (EMA and the 115D8 antigen).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased expression of cellular markers in Epstein-Barr virus-positive Hodgkin's disease. 752 10

When graft-versus-host (GVH) disease affects the liver, it is characteristically the bile ducts which are involved, infiltrated by lymphocytes. To characterize this process further, and to determine whether there were any antigenic changes in the bile ducts, we stained 9 liver biopsies involved by GVH disease, 10 non-GVH biopsies that had a prominent portal lymphocytic component, and 8 biopsies taken incidentally at surgery for noninflammatory liver disease with epithelial membrane antigen, AE-3, AE-1, a keratin cocktail, keratin 19, CD45RO (UCHL-1), CD43 (Leu-22), CD20 (L26), vimentin, and LN-3. The infiltrating lymphocytes were T cells (CD45RO+, CD43+, CD20-) which variably expressed LN-3. The bile ducts were positive for the keratin cocktail, AE-1, AE-3, and keratin-19, but only occasionally positive for EMA and LN-3. There was no significant difference in the staining patterns of either the bile duct cells or lymphocytes between the three groups. With the antibodies that we used, there does not appear to be a significant difference in the antigenic phenotype of the bile ducts in GVH as compared to normal or reactive livers.
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PMID:Phenotype of bile ducts and infiltrating lymphocytes in graft-versus-host disease. 768 95

20 specimens of normal pleural mesothelium were investigated with six lectins using isolated cells and tissue specimens as well as two different fixation techniques (glutaraldehyde and formaldehyde) and 10 monoclonal antibodies (MAb) on cytologic preparations only. Lectin binding sites for ConA, WGA, and PNA were present in all cases, whereas binding sites for the lectins HPA, SBA, and UEA-I could never be found. There was no staining difference with the two preparation and fixation techniques proving that they may be used to compare directly histologic and cytologic studies. Ten of fourteen histologic specimens were positive for the blood group antigen Lewis(y), three of them were positive for the antigen Lewis(b), all fourteen specimens were negative for Lewis(a) and Lewis(x). In all cases, mesothelial cells expressed ICAM1 and pancytokeratin. The antibodies against EMA, CEA, CD24, CD15, CD20, CD5, and HEA125 showed no reaction in mesothelial cells. Because HPA, UEA-I, SBA as well as CEA and HEA125 react in a high percentage with adenocarcinomas, non reactive cells of pleural effusions negative with these markers may be confidentially considered to be mesothelial in origin.
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PMID:Lectin binding sites and immunocytochemical characterization of normal pleural mesothelium. 854 94

This study compares the histologic and immunophenotypic features of 71 cases of primary CD30+ diffuse large-cell lymphomas (DLCL) and 128 cases of Hodgkin's disease (HD) and discusses the clinical features of 52 patients with CD30+ DLCL. It includes analysis of sites of involvement, staging, response to treatment, sites and treatment of recurrences, and disease-free and overall survival. Diagnostic immunophenotypic differences were found between CD30+ DLCL and HD. All cases of CD30+ DLCL were positive for one or more common or lineage-specific lymphocyte antigens or for EMA. In contrast, 96.9% of HD cases were negative for CD45, CD45-RO, CD43, and CD20. The four exceptions are discussed. All cases of HD were negative for EMA. In patients with CD30+ DLCL, a T-cell phenotype was found in 60%, a null-cell type in 22%, and a B-cell type in 18% of the cases. The median age of patients with T- and null-cell phenotype was 22 years (range, 4 to 72). Fifty-two percent of them had high-stage (III and IV) disease and 61% had extranodal involvement at presentation, including 25% with skin lesions. Lymph nodes draining the skin lesions became involved in seven of 11 patients. No patient had initial bone marrow involvement. Most patients were treated with chemotherapy, and 83% had a complete remission. Fifty-four percent remain free of disease with a median follow-up of 47 months. Thirteen patients (29%) had one or more recurrences and five of them remain free of disease after salvage therapy, with a median follow-up period of 79 months. The clinical stage did not affect survival, probably as a result of different therapy. The t(2;5) translocation was found in five of 15 patients who had cytogenetic abnormalities. Of the other 10 cases, the translocation was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) in four of five cases studied. All nine cases were of T- or null-cell phenotype. The cases of B-cell CD30+ DLCL had a characteristic immunophenotype. All were negative for EMA. These patients were older and had frequent bone marrow involvement but no skin infiltration by lymphoma. All three patients who were human immunodeficiency virus-positive (HIV+) had lymphomas of B-cell lineage. Detection of the t(2;5) translocation by molecular genetics is a useful and highly specific marker in the differential diagnosis between HD and CD30+ DLCL.
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PMID:CD30 (Ki-1)-positive malignant lymphomas: clinical, immunophenotypic, histologic, and genetic characteristics and differences with Hodgkin's disease. 863 11

T-cell-rich B-cell lymphoma (TCRBCL) is an unusual lymphoma which is difficult to diagnose. A majority of reactive T-cells and numerous histiocytes mask the few large neoplastic B-cells. Fourteen cases of TCRBCL were studied in order to identify the main histological and cytological features useful for this diagnosis. Neoplastic cells are atypical and sometimes difficult to classify. Several types are seen; they are mostly centroblasts, which represent more than 50% of the tumour cells but are sometimes multilobated, immunoblasts- or Reed-Sternberg-like cells. Interestingly, at least two, and often three, types of tumour cell are present in all the cases. Epithelioid cells and histiocytes are always found and are often numerous. Hypervascularization and fibrosis are present in the majority of cases, but without annular bands. Necrosis is absent. All tumour cells express CD20 but EMA is expressed in less than half the cases. In two cases, the association of a diffuse large B-cell lymphoma in one site and a TCRBCL in another suggests that TCRBCL may be considered as a peculiar pattern of a diffuse large B-cell lymphoma with a strong stroma reaction. TCRBCL may not represent a clinicopathological entity.
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PMID:Morphological variability of tumour cells in T-cell-rich B-cell lymphoma. A histopathological study of 14 cases. 897 60

A 21-year-old man who had anaplastic large cell lymphoma (ALCL) of the null-cell type with multiple bone involvement is reported. On admission, he had symptoms of incomplete paraplegia and urinary and rectal incontinence. Workup studies for staging revealed para-aortic lymph node swellings and multiple bone involvement including skull, ribs, left iliac bone, and thoracic/lumbar spine. Because paraplegia was rapidly progressive, a decompression operation was performed. The biopsy specimen obtained from the lumbar spine revealed sheetlike proliferation of anaplastic large cells. These cells were positive for CD30 (Ki-1), EMA, vimentin, and p80NPM/ALK, and negative for CD3, CD20 (L26), and CD45 (LCA). Epstein-Barr virus-encoded small RNAs were not detectable in these cells. Thus, the patient was diagnosed as having ALCL of the null-cell type. He was treated with several courses of combination chemotherapy, and finally with total body irradiation plus high-dose chemotherapy supported by peripheral blood stem cell transplantation. However, soon after the treatment, the lymphoma cells massively infiltrated his bone marrow. He died of lymphoma 8 months after admission.
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PMID:Anaplastic large-cell lymphoma of null-cell type with multiple bone involvement. 987 67

To determine whether there might be immunophenotypic differences between nodular lymphocyte predominance Hodgkin's disease (NLPHD) and progressive transformation of germinal centers (PTGC) to aid in the differential diagnosis, we compared 16 cases of NLPHD with 13 cases of florid PTGC and 2 cases of focal PTGC. Paraffin-section immunohistochemistry was performed for CD20, CD45RA, CD45RO, CD3, CD43, CD57, EMA, CD30, and CD21. All PTGC cases showed well-circumscribed nodules of confluent sheets of CD20+ CD45RA+ small cells. T cells were scattered singly or in small groups. In 5 patients with florid PTGC, the T cells in some of the nodules formed rings around a few large transformed lymphocytes. In contrast, the nodules in all NLPHD cases showed an irregular, "broken-up" pattern with CD20 and CD45RA, and there were prominent T cell rosettes around the CD20+ large cells in all nodules. Rosettes of CD57+ cells and staining of large cells for EMA were seen in 3 and 2 cases of NLPHD, respectively, but not in PTGC. There were no differences between NLPHD and PTGC with respect to staining for CD30 or CD21. Three of the eight patients with florid PTGC and a few T cell rosettes had had persistent or recurrent lymphadenopathy; NLPHD developed in 1 of these patients 13 years later. We conclude that a combination of pan-B and pan-T antigens can be a useful adjunct to morphology in distinguishing NLPHD from PTGC. In approximately one-third of florid PTGC cases, T cell rosettes may be present, but they are notably fewer than those in NLPHD. Close follow-up of such patients may be appropriate.
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PMID:Progressive transformation of germinal centers and nodular lymphocyte predominance Hodgkin's disease: a comparative immunohistochemical study. 988 1

Follicular dendritic cell tumors are uncommon and usually occur in lymph nodes. We report the case of a follicular dendritic cell tumor that occurred in the palate of a 14-year-old boy and manifested itself as a nodular mass. Histologically, the neoplasm consisted of spindle-shaped or oval-shaped cells with eosinophilic cytoplasms and nuclei with delicate, dispersed chromatin. The lesional cells were principally arranged in diffuse, fascicular patterns with vaguely whorled or storiform areas. Focal multinucleate tumor giant cells and lymphocytes were observed throughout the neoplasm. Immunohistochemically, tumor cells were positive for the follicular dendritic cell markers CD21, CD35, and CD23 and for S-100 protein, CD68, and muscle-specific actin. Tumor cells were negative for LCA, CD20, EMA, CK (AE1/AE3), HMB45, and CD34. Lymphocytes were positive for LCA and CD45RO. Although follicular dendritic cell sarcoma is a very uncommon tumor, it should be included in the differential diagnosis of tumors in this location.
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PMID:Extranodal follicular dendritic cell sarcoma of the palate. 1005 77

A high-quality approach to lymphoproliferative diseases needs mastering the basic principles of morphology, immunology and genetics. The diagnosis relies on both traditional methods (histopathological analysis) and modern procedures (supported by advanced techniques such as immunohistochemistry, flow cytometry, and molecular biology). This paper presents a personal point of view developed by the author as a consequence of experiencing the immunohistochemical reactions for the diagnosis of non-Hodgkin's malignant lymphomas. Immunohistochemistry, as an effective and currently practiced procedure, allows the identification of the cellular line of the proliferating cells. Full details are given for material and methods, providing a complete characterization of the used monoclonal antibodies (DAKO-CD20, L26, DAKO-CD3, DAKO-CD68, PG-M1, DAKO-E29, EMA), as well as an integral description of the sequenced working phases. Relevance, efficiency, performance, limits and perspectives of the employed procedure are discussed with direct references to the results of this personal study.
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PMID:[The importance of immunohistochemical examination in the diagnosis of malignant lymphoproliferative diseases--the author's personal experience]. 1075 84


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