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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 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

While L26 (CD20) is now well established as a B-cell marker of high specificity for use in paraffin-embedded tissues, paraffin-reactive T-cell antibodies (UCHL1, MT1, Leu-22, DF-T1, and MT2) have not shown comparable lineage specificity. A new commercially available polyclonal antibody directed against a synthetic peptide sequence of the CD3 (T-cell) antigen has recently become available for use on paraffin sections. In order to evaluate the utility of this antibody, we studied CD3 expression in conjunction with L26 and leukocyte common antigen (LCA) in 15 T-cell and 20 B-cell non-Hodgkin's lymphomas (NHL), all genotypically confirmed by DNA hybridization and immunophenotyped by immunoperoxidase studies in frozen tissue. Ten of 15 T-cell NHLs (67%) showed unequivocal immunolabeling of neoplastic cells with anti-CD3 in paraffin-embedded tissue. Of the five negative cases, three were lymphoblastic lymphomas, and two were peripheral (postthymic) lymphomas (one anaplastic large cell, Ki-1 positive and one large cell, immunoblastic). CD3 expression was identical in paraffin and cryostat sections (100% concordance). Twenty of 20 B-cell NHLs were positive with L26 and LCA but were negative with anti-CD3. Other neoplasms examined, including three granulocytic sarcomas and 45 nonhematopoietic tumors, were similarly negative with anti-CD3. We conclude that polyclonal anti-CD3 is a sensitive and highly specific T-cell marker in paraffin-embedded tissue and, when used in conjunction with LCA and L26, that it can determine cell lineage in the majority of non-Hodgkin's lymphomas.
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PMID:Methods in pathology. Identification of T-cell lymphomas in paraffin-embedded tissues using polyclonal anti-CD3 antibody: comparison with frozen section immunophenotyping and genotypic analysis. 182 34

Several monoclonal antibodies (MoAbs) are now available for immunophenotyping non-Hodgkin's lymphomas (NHLs) in paraffin-embedded tissue sections. To determine the reliability of these reagents in predicting the genotype, 44 cases of NHL were studied with the alkaline phosphatase-anti-alkaline phosphatase technique with the use of the following MoAbs: leukocyte common antigen (CD45), Mac 387, L26, 4KB5, MB1, MB2, LN2, UCHL1, MT1, and MT2. The lineage of the neoplastic cells was determined in all cases by gene rearrangement studies for immunoglobulin heavy chain and for the T-cell receptor beta-chain. Genotypic results showed B-cell lineage in 33 cases (75%), T-cell lineage in 6 cases (14%), and mixed or undetermined lineage in 5 cases (11%). A concordance of lineage assignment by paraffin section immunophenotyping with gene rearrangement studies was observed in 37 of 39 (95%) lymphomas with an unequivocally defined genotype. MoAb L26 was the most sensitive in detecting B-cell genotype; MoAbs MT1 and UCHL1 were the most sensitive and specific, respectively, in detecting T-cell genotype. The authors conclude that lineage assignment of NHLs in paraffin sections is reflective of the corresponding genotype when an appropriate panel of MoAbs is used.
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PMID:Immunophenotyping of non-Hodgkin's lymphomas in paraffin-embedded tissue sections. A comparison with genotypic analysis. 184

Reports of sinonasal non-Hodgkin's lymphomas, analysed with monoclonal antibodies, are scarce, and differentiation of these lymphomas from Wegener's granulomatosis can be difficult. In this study, we investigated histopathologically and immunohistologically 20 cases of non-Hodgkin's lymphoma, primary in the sinonasal region, and sinonasal biopsies from 11 patients with Wegener's granulomatosis. All T-cell lymphomas (n = 7) and plasmacytomas (n = 4) were stage I at clinical presentation, while all B-cell lymphomas (n = 9) presented at higher stages. T-cell lymphomas tended to be more frequent in the nasal cavity and paranasal sinuses; B-cell lymphomas more often presented in the nasopharynx. Remarkably, 1 B-cell lymphoma expressed MT1, and 1 T-cell lymphoma expressed L26 (CD 20). The follow-up of 2 patients with a clinical diagnosis of Wegener's granulomatosis was suggestive of non-Hodgkin's lymphoma. Retrospective immunohistochemical analysis revealed that the original histological diagnosis of non-specific inflammation had to be changed to T-cell lymphoma, pleomorphic small cell type. We conclude that a biopsy from the sinonasal region with a dense inflammatory infiltrate, consisting predominantly of T-lymphocytes, renders a diagnosis of Wegener's granulomatosis unlikely and is at least suspicious of T-cell lymphoma. Immunohistochemical analysis is warranted for this type of biopsy.
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PMID:Sinonasal non-Hodgkin's lymphomas and Wegener's granulomatosis: a clinicopathological study. 190 Sep 69

Eight antibodies (UCHL1 (CD45RO), MT1 (CD43), MT2 (CD45R), 4KB5 (CD45R), MB1 (CD45R), MB2, L26 (CD20) and LN1 (CDw75)) have been examined for reactivity with routine specimens of normal and hyperplastic lymphoid organs (n = 6), non-Hodgkin's lymphomas (n = 62), Hodgkin's disease (n = 27) and non-lymphoid malignancies (n = 9). In normal and hyperplastic lymphoid organs, UCHL1 and MT1 stained predominantly T cells; 4KB5, MB1, MB2, L26 and LN1 stained predominantly B cells; and MT2 reacted with a subset of B and T cells. The lineage of the neoplastic cells was correctly identified in 24 of 28 (86%) peripheral T-cell lymphomas; and in 31 of 35 (88%) B-cell malignancies. In two cases of lymphocyte-predominant Hodgkin's disease, the Hodgkin's and Reed-Sternberg (H&RS) cells were 4KB5+, L26+ and/or LN1+. The H&Rs cells in nodular sclerosis and mixed cellularity Hodgkin's disease were positive with 4KB5 in 17 of 25 cases. Antibodies UCHL1, MT1, MB1, MB2, L26 and LN1 also labelled some H&RS cells, but in a much smaller proportion of the cases. In three of nine non-lymphoid neoplasms, UCHL1 and MB2 showed a staining of the neoplastic cells, but the staining was cytoplasmic rather than membrane-associated. The remaining antibodies were unreactive with the non-lymphoid malignancies. It is concluded that many non-Hodgkin's lymphomas can be typed in routine specimens, and that antibodies UCHL1, MT1, L26 and LN1 are especially useful in this respect. The antibodies do not provide a means of distinguishing between non-Hodgkin's lymphomas and Hodgkin's disease.
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PMID:Use of monoclonal antibodies for the typing of malignant lymphomas in routinely processed biopsy samples. 206 5

OPD4 is a recently described monoclonal antibody that recognizes a fixation-resistant 200 kD antigen restricted to a subset of T cells. Immunolabelling with OPD4 in paraffin sections of normal lymphoid tissues and cases of malignant lymphoma was compared with that of other antibodies in common use, including the T-cell restricted antibodies MT1 and UCHL1 and the B-cell restricted antibodies MB1, F8-11-13, and L26. OPD4 showed similar immunoreactivity to UCHL1 in normal tissues. OPD4 did not stain Reed-Sternberg cells in Hodgkin's disease. In non-Hodgkin's lymphomas, OPD4, like UCHL1, reacted with only 2/22 B-cell lymphomas. OPD4 was, however, less useful as a marker of T-cell lymphomas, staining only 11/32 cases, while UCHL1 stained 22/32 cases. We conclude that OPD4 is not a useful antibody for the routine diagnosis of T-cell lymphoma.
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PMID:Immunohistological analysis of the immunoreactivity of normal lymphoid cells and lymphomas with the monoclonal antibody OPD4. 207 11

Several immunohistochemical methods are now available for the staining of neoplastic cells in tissue sections. The authors have found that the alkaline phosphatase-anti-alkaline phosphatase (APAAP) method is sensitive and reliable. Murine monoclonal or nonmurine polyclonal antibodies can be used to label a variety of membranous and/or cellular constituents in tissues that have been routinely processed in a histopathology laboratory. The monoclonal antibody against leukocyte common antigen (CD45) can be used to differentiate hematologic from nonhematologic tumors. Monoclonal antibodies (L26, LN1, LN2, LN3, MB1, MB2) label B-cell lymphomas, whereas other monoclonal antibodies (UCHL1, MT1) more characteristically stain T-cell lymphomas. Polyclonal antibodies against CD3 specifically mark neoplastic cells from T-cell lymphomas and leukemias but as yet are not commercially available. Monoclonal antibodies Leu-M1 (CD15), Ber H2 (Ki-1; CD30), and LN2 label Reed-Sternberg cells from most cases of nodular sclerosis, mixed cellularity, and lymphocyte-depleted Hodgkin's disease. Monoclonal antibodies Mac 387, KP1 (CD68), and NP57 (antielastase), as well as polyclonal antibodies against lysozyme, help identify subtypes of acute myeloid leukemia and extramedullary myeloid cell tumors. Although there are now excellent reagents ready for use, there is still a significant need for more lineage-specific (particularly against CD epitopes) monoclonal antibodies capable of labeling neoplastic cells in paraffin-embedded tissue sections from patients with hematologic malignancies.
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PMID:Immunophenotyping of hematologic neoplasms in paraffin-embedded tissue sections. 218 Feb 77

Five cases of nodular, lymphocyte predominant Hodgkin's disease (nLP HD), in which an association with (n = 3) and transformation to (n = 2) large cell lymphoma (LCL) were found, were studied with monoclonal antibodies against B-, T-, and Reed-Sternberg (R-S) cell-associated antigens and epithelial membrane antigen (EMA) on paraffin sections. Both lymphocytic (L) and histiocytic (H) cells of nLP HD and lymphoma cells of LCL expressed multiple B-cell-associated antigens (detected by LN-1/CDw75, L26, MB2, DBB.42, DBA.44, DND.53, DNA.7 antibodies) but did not react with antibodies against T-cell-associated (MT1, UCHL1/CD45RO) (one exception for CD45RO in LCL) and R-S cell-associated (Leu-M1/CD15, Ber-H2/CD30) antigens. EMA was expressed by L and H cells in all cases and conserved in LCL cells, emphasizing the frequent expression of EMA by the diagnostic cells of nLP HD. An antibody (BNH9) against blood group-related antigens (H and Y oligosaccharide antigens) that does not normally react with lymphoid cells was found to be reactive with few L and H cells in two of five and most LCL cells in four of five cases. The finding might be indicative of abnormal activation of lymphoid cells. The data reinforce current implications that nLP HD is a B-cell malignancy in evolution and that it is not truly representative of Hodgkin's disease in terms of biological and clinical behavior.
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PMID:Further phenotypic evidence that nodular, lymphocyte-predominant Hodgkin's disease is a large B-cell lymphoma in evolution. 224 Mar 55

Lymph node biopsies from 57 local and referred cases, previously diagnosed at Southampton between 1978 and 1987 as lymphocyte predominance Hodgkin's disease were examined using the monoclonal antibodies MT1, UCHL1, L26, LN-1, E29/68 (EMA), Leu-M1 (CD15) and Ber-H2 (CD30). Of the 34 cases with a nodular architecture, 21 (19 male, two female) contained polylobated Reed-Sternberg cell variants with a B-cell phenotype, which lacked expression of CD15. In all cases, the polylobated cells showed positive staining with L26 and LN-1. Six cases expressed EMA and three showed positive staining with Ber-H2. Two cases lacking polylobated cells were reclassified as reactive follicular hyperplasia with progressive transformation of germinal centres. The remaining 11 cases had an atypical immunophenotype and were reclassified, mainly as mixed cellularity Hodgkin's disease. In six cases, the lymph node architecture showed a mixture of nodular and diffuse growth patterns. Five of these cases contained polylobated cells with the typical morphology and immunophenotype of those seen in nodular lymphocyte predominance Hodgkin's disease. The sixth case contained cells expressing CD15, and was reclassified as nodular sclerosing Hodgkin's disease. Of the fifteen biopsies with a diffuse architecture, four contained polylobated B-cells lacking expression of CD15. These were considered to be diffuse lymphocyte predominance Hodgkin's disease. The remaining 11 cases were reclassified as either Hodgkin's disease, mixed cellularity or as T-cell lymphomas.
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PMID:Lymphocyte predominance Hodgkin's disease--an immunohistochemical study. 232 37

The present report describes the results of a combined morphological, enzyme- and immunohistochemical analysis of nine cases of malignant non Hodgkin's lymphomas (NHL) clinically presenting as lethal midline granuloma. In a previous report written before antibodies directed against B and T lymphocytes were available, a histiocytic origin of such neoplasms had been suggested. A panel of antibodies reactive with most B cells (L26, MB1, KiB3) and a majority of T cells (MT1, UCHL1) was applied on paraffin sections of formalin fixed tissues as well as antibodies directed against leukocyte common antigen (LCA), myeloid/histiocyte antigen (MAC 387), lysozyme, alpha-1-antitrypsin, alpha-1-antichymotrypsin, S-100 protein, prekeratin and immunoglobulin light chains. Enzyme histochemistry included tests for non-specific acid esterase, acid phosphatase, beta-glucuronidase and chloroacetate esterase. As a result, five T, two B and two unclassified (malignant histiocytosis probable) NHL were identified, indicating distinct heterogeneity of NHL as causative disorders in lethal midline granuloma.
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PMID:Heterogeneous malignant non Hodgkin's lymphomas as a causative disorder in lethal midline granuloma. 252 38


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