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)

Monoclonal antibodies (mAbs) directed against the leucocyte common (CD45) antigen have been proposed as a useful tool for the differential diagnosis between malignant lymphomas (CD45+) and poorly differentiated nonhemopoietic tumors (CD45-). Thanks to the availability of mAbs directed against fixative-resistant epitopes of the CD45 molecule, this distinction can now easily be made even in routinely processed tissues. However, a small percentage of morphologically poorly defined neoplasms are difficult to diagnose even with the help of immunohistochemistry. The investigators report that 63 out of 165 anaplastic large-cell (ALC) lymphomas did not show any reactivity for the CD45 antigen in paraffin sections. In routine biopsies, the lymphomatous nature of these cases, most of which had been sent for consultation, could be always unequivocally established by demonstrating negativity for cytokeratins (mAb KL1) and clear dot-like and/or surface reactivity with the Ber-H2 mAb, which is directed against a fixative-resistant epitope of the lymphoid cell activation antigen CD30. Strikingly, 54% of the CD45-cases reacted with mAbs directed against fixative-resistant epitopes of the T cell-restricted CD45RO antigen (mAb UCHL1) or the B-restricted molecules CD45RA (mAb 4KB5) and L26 (unclustered). In order to avoid confusion of ALC lymphomas with anaplastic nonlymphoid tumors, pathologists must be aware of the existence of CD30+/CD45- ALC lymphomas, as they can mimic the above-mentioned malignancies both morphologically (due to the sinusoidal growth pattern) and phenotypically (due to the expression of EMA). The investigators conclude that the combined use of mAbs directed against fixative-resistant epitopes of the CD30, CD45RO, CD45RA, and L26 antigens and cytokeratins is essential for the correct diagnosis and treatment of these equivocal cases.
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PMID:Variable expression of leucocyte-common (CD45) antigen in CD30 (Ki1)-positive anaplastic large-cell lymphoma: implications for the differential diagnosis between lymphoid and nonlymphoid malignancies. 169 92

The authors studied the immunophenotype of nine sinonasal lymphomas using a panel of monoclonal antibodies that react with fixed, paraffin-embedded material (EMA, CAM 5.2, CD45, CD37 [MB-1], MB-2, L-26, CDw75 [LN-1], CD45RA [4 KB-5], CD43 [MT-1], and CD45RO [UCHL-1]). There were seven men and two women, with a mean age of 64 years (range, 9-89 years) and median age of 56 years. Three tumors were limited to the nasal cavity, and the other six had multiple sites of involvement, including the nasal cavity (five), antrum (six), ethmoid (two), orbit (two), and hard palate (one). Histologically, one was a lymphoblastic lymphoma (LBL), one was small cleaved-cell lymphoma (SCCL), three were mixed-cell lymphomas (MCLs), and four were large cell lymphomas (LCLs). Four cases were T-cell lymphomas (one SCCL, three MCLs), four were B-cell neoplasms (four LCLs), and one was of uncertain lineage (LBL). Angioinvasion, coagulative necrosis, and epitheliotropism were seen in the T-cell lymphomas. Extranasal dissemination was seen in four cases: one LBL that involved the lymph nodes, skin, and testes 15 months after diagnosis; one B-LCL that involved the skin 9 months after diagnosis; and one B-LCL and one T-MCL that involved the gastric mucosa and lung simultaneously with nasal presentation. This study shows a higher predominance of B-cell lymphomas in the sinonasal region than previously reported in Oriental populations. However, the T:B ratio of these lymphomas is still greater than that observed for primary lymph node-based neoplasms.
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PMID:Non-Hodgkin's lymphomas of nasal cavity and paranasal sinuses. An immunohistochemical study. 186 73

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

B5-fixed/paraffin-embedded Jamshidi needle biopsies from 125 multiple myeloma patients were reviewed according to both morphological and immunohistological criteria. At microscopic examination, the following parameters were evaluated: i) grade of malignancy (low = 56; intermediate = 50; high = 19); ii) growth pattern (interstitial +/- sheets/nodules = 90; nodular = 13; packed marrow = 18; sarcomatous = 4); III) histological stage (I = 64; II = 35; III = 26). Comparison of the findings in trephine biopsies and aspirates showed that in 30% of the cases the latter led to an underestimation of the tumor burden. Immunohistochemical determination of Ig easily allowed: i) differential diagnosis from exuberant reactive plasmacytosis; ii) recognition and counting of neoplastic plasma cells; iii) detection of minimal residual disease after treatment. Immunohistochemistry also confirmed phenotypic aberration of neoplastic plasma cells, showing positivity for CD45, EMA, and cytokeratins in 14%, 59%, and 25% of the cases, respectively. Furthermore, it displayed expression of the P-glycoprotein in 4/8 resistant cases. These findings underline that routinely processed Jamshidi needle biopsies can be of great value in the study of patients with multiple myeloma.
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PMID:Histology and immunohistology of bone marrow biopsy in multiple myeloma. 262 92

A novel, comprehensive panel of monoclonal antibodies was tested in a large series of routinely processed lymph node biopsy specimens from patients with Hodgkin's disease (69 cases), with the object of developing either definitive or adjunctive diagnostic criteria. B- and T-cell lymphomas and reactive states that could mimic Hodgkin's disease were also assessed with the same monoclonal antibody panel. In addition to the popularly used anti-Leu-M1 (CD15), the panel included the recently produced Ber-H2 (CD30) antibody, which detects a formalin-resistant epitope of the Ki-1 antigen. The other monoclonal antibodies were directed against epithelial membrane antigen (Dako-EMA) and leukocyte common antigen (Dako-LC) (CD45), as well as B-cell (LN-1 and LN-2) and T-cell (MT1) associated antigens. The results showed clear phenotypic separation of nodular lymphocyte predominant subtype of Hodgkin's disease from other subtypes. The lymphocytic and histiocytic cells of nodular lymphocyte predominant Hodgkin's disease were reactive for LN-1 (all cases) and anti-EMA (most cases) but negative for anti-Leu-M1 and Ber-H2. Within the other subtypes--i.e. nodular sclerosis and mixed cellularity--nearly all Reed-Sternberg cells and Hodgkin's cells were positive for both anti-Leu-M1 and Ber-H2. Ber-H2 monoclonal antibody was observed to react more frequently with Reed-Sternberg cells and Hodgkin's cells in Bouin's- or formalin-fixed tissues. Pleomorphic T-cell lymphomas, which could mimic Hodgkin's disease on morphology, created the same problem on phenotypic analysis. However, MT1 identified a significant proportion of T-cell lymphomas with Reed-Sternberg-like cells, having proven negative for Reed-Sternberg cells and Hodgkin's cells in Hodgkin's disease. Thus, a combination of anti-Leu-M1, Ber-H2, anti-EMA, LN-1, and MT1 monoclonal antibodies appears at present to be the most useful panel for the diagnosis and the differential diagnosis of Hodgkin's disease.
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PMID:Monoclonal antibodies in the diagnosis of Hodgkin's disease. The search for a rational panel. 282 35

Reagents that recognize antigens on lymphoid cells in fixed and wax-embedded sections have been applied to a series of cases of non-Hodgkin's lymphomas. The panel consisted of MB1, 4KB5 (CD45r), LN1, L26 and MB2 which recognize antigens expressed predominantly on B-lymphocytes; UCHL1 and MT1 which recognize antigens expressed on T-lymphocytes and myeloid cells; antibodies recognizing the non-lineage antigens LeuM1 (CD15), BerH2 (CD30), anti-EMA; anti-lysozyme and MAC 387 which detect antigens present on some macrophages; and finally TAL1B5 (class II MHC), CAM 5.2 (low molecular weight cytokeratin) and PD7/26 + 2B11(CD45). Two hundred and four cases of non-Hodgkin's lymphoma have been studied, of which 158 had been fully characterized on frozen sections. The series was biased towards high-grade (n = 108) and T-cell (n = 44) tumours and these were largely prospectively accrued. It was found that discrimination between B-cell and T-cell lymphomas can be reliably achieved using these reagents and that a small panel (CD45, L26, MB2, MT1, UCHL1) is adequate for this purpose. Using the full range of reagents it is not possible to subdivide cases into groups that correspond with morphological subtypes of lymphoma. Although paraffin section immunohistochemistry is of value, the diagnosis of lymphoproliferative disorders must still be based upon the assessment of well fixed, carefully prepared tissue sections using conventional tinctorial methods.
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PMID:Paraffin section immunohistochemistry. I. Non-Hodgkin's lymphoma. 326 64

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

A case of aggressive plasma cell leukemia with unusual morphological and cytogenetic features is reported. A 65-year-old man was admitted to hospital due to anemia, thrombocytopenia, and renal insufficiency. Bone marrow examination and peripheral blood smear revealed a large number of pleomorphic cells with convoluted and multilobulated nuclei. Immunohistochemistry of the bone marrow biopsy was negative for anti-keratin antibodies CAM.5.2 and AE1/AE3, but positive for EMA. The immunophenotypic features of these cells were suggestive of plasma cell origin with positivity for CD38, CD56, CD9, and CD44 and a weak positivity for CD71 and CD45 (40% of the cells), while all other markers of hematopoietic origin were negative. Furthermore, a serum protein electrophoresis showed a monoclonal component type IgG-kappa of 70 g/l. The cytogenetic analysis demonstrated a hypotetraploid clone with multiple numerical and structural abnormalities. Although some of the aberrations found are associated with plasma cell malignancies--e.g., structural rearrangement of chromosome 1, del(6q), and monosomy 13--the karyotypic complexity in the present case is unusual. The course of the disease was very aggressive, and the patient died 3 days after admission.
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PMID:Aggressive course of primary plasma cell leukemia with unusual morphological and cytogenetic features. 853 63

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

Fifty-three consecutive cases of adult CD30+ anaplastic large cell lymphoma (ALCL) have been analyzed. Thirty-six were classified as Hodgkin's disease like variety (HL) (67%) and seventeen as so-called common type (CT) (33%). All cases strongly expressed the CD30/Ki-1 antigen; the neoplastic cells expressed CD15, CD45 and EMA in 60%, 44% and 33% of cases, respectively; T. B and null phenotypes were found in 37%, 17% and 46% of cases. Bulky mediastinal, B symptoms, and extranodal disease at diagnosis were present in 36%, 49% and 25% of cases. EBV encoded latent membrane protein (LMP-1) was found in 10 cases. Of the 13 tested cases only 4 expressed a weak positivity of the CD40 molecule, in a fraction of the tumor cells; in the same cases CD21 was never found. Patients were treated with various protocols; of the 50 evaluable patients, 39 (78%) obtained a complete remission (CR), 3 (6%) a partial remission (PR) and 8 (16%) did not respond. The projected overall disease free survival (DFS) at 36 months is 70%. Only patients with advanced disease stage (III-IV) showed a statistically decreased DFS and survival. Only symptomatic and extranodal disease significantly appeared to influence survival. This study confirms the good outcome of this group of lymphomas and differs from other reports for some clinical (lower percentage of advanced stage, extranodal disease and skin infiltration) and pathological (HL/CT ratio and immunophenotype) features.
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PMID:Anaplastic large cell lymphoma: a clinicopathologic study of 53 patients. 881 81


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