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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

Sixty three cases of Hodgkin's disease are studied (two with lymphonodular predominance, 15 with diffuse lymphocyte predominance, 26 nodular sclerosis, 15 mixed cell and 5 lymphocyte depletion) with a panel of 8 monoclonal antibodies, material routinely used and included in paraffin: Ber H2 (CD30), Leu M1 (CD15), Common Leukocyte Antigen (CD45), L26 (CD20), MB2, UCHL1 (CD45 RO), MTI (CD43) and Epithelial Membrane Antigen. Ber H2 turned out to be the most usefull marker, positive in 100% of cases, independently of the histologic type. Positiveness with Leu M1 ranged from 100% (2/2 cases) of lymphonodular predominance, to 53.3% (8/15 cases) of diffuse lymphocyte predominance. The reactivity of the rest was variable, 1 though it is note worthy the positiveness of B markers (L26, MB2) in the two cases with lymphonodular predominance. In the other subtypes, reactivity with L26 was greater than that with MB2. T cell marker expression was minimal, except for the positiveness in 40% of cases (2/5) of the lymphocyte depletion type. In addition, the results of other series are revised and as a result the possible histogenesis of Hodgkin's disease is discussed.
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PMID:[The immunological characterization of 63 cases of Hodgkin's disease with a panel of 8 antibodies]. 137 67

Morphological and immunohistological studies were carried out on a series of 137 lymphomas including CD30+ anaplastic large cell (ALC) lymphomas (48 cases) and non-lymphocyte predominant Hodgkin's disease (HD) (89 cases), with the aim of assessing in situ expression of a combination of antibodies including anti-CD30/BerH2, epithelial membrane antigen (EMA), CD15 and CD45, in addition to other monoclonal antibodies suitable for paraffin tissues. A greater proportion of cases of ALC lymphomas than of HD exhibited positivity for CD45 (91.7% vs 17.6%), EMA (56.2% vs 4.5%), CD43 (53.6% vs 13.1%) and CD45RO (39.5% vs 3.5%), whereas Reed-Sternberg (RS) cells in HD most frequently expressed CD15 (93.2% vs 20.8%) antigen. Moreover, in 35 of 48 (72.9%) ALC lymphomas tumour cells expressed the CD30+, CD45+, CD15-, EMA- or + phenotypic profile, while in the same percentage (62/85) of HD cases RS cells were found to express the CD30+, CD45-, CD15+, EMA- profile. This study suggests that the differential expression of CD45, EMA, and CD15 may be used in the separation of ALC lymphomas and HD. However, co-expression of CD30, CD45 and CD15 antigens by RS cells in HD (14/85 cases, 16.5% in this series) and by tumour cells in ALC lymphomas (9/48 cases, 18.7% in this series) may be encountered in a non-negligible fraction of cases.
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PMID:Paraffin section immunohistochemistry in the diagnosis of Hodgkin's disease and anaplastic large cell (CD30+) lymphomas. 137 44

Adhesion molecules play an important role in the functioning of the immune system, particularly with regard to cell-cell interactions and antigen presentation. Several adhesion molecules are expressed on Hodgkin's disease-derived cell lines and these are important in their molecular interactions as antigen presenting cells (APC). There are no data regarding the expression of many of these adhesion molecules on Reed-Sternberg cells and its mononuclear variant (Hodgkin's cells (HC)) present in pathological material. To obtain this information we undertook an immunohistological study on material from 18 cases of Hodgkin's disease using a panel of MoAbs to examine the expression of adhesion molecules on HC. The HC were shown to express the integrin beta 1 subfamily molecules, LFA-1 (CD11a) and p150,95 (CD11c) in high density but lacked CR3 (CD11b). All of the immunoglobulin gene superfamily adhesion molecules studied were present to some degree on HC, with ICAM-2, in particular, showing moderate to strong expression in most cases. The Hermes antigen CD44 was present in high density but leukosialin (CD43), another molecule present on diverse leucocyte types, was, in general, not detected on HC. These new data showing that ICAM-1, ICAM-2 and LFA-3 are, like LFA-1, expressed on HC emphasize the ability of HC to act as APC. The known adhesion molecule phenotype of the recently defined haematopoietic lineage of human dendritic cells (DC) is broadly similar to that of HC, perhaps supporting the hypothesis that some HC represent a malignancy of an APC (DC) lineage.
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PMID:Hodgkin's cells express a novel pattern of adhesion molecules. 139 91

Histologically diagnosed, or in part questionable, malignant pleomorphic peripheral T-cell lymphomas (pPTCLs, n = 16) and mixed-cellularity Hodgkin's disease (MCHD, n = 12) were objectively compared by the use of combined immunohistochemistry on paraffin sections, test-point analysis of tissue components, and semi-automated nuclear morphometry on semi-thin resin sections. Classical, qualitative histomorphological distinction of these sub-types of lymphomas proved to be valid and is probably still the best method. Quantitative discriminant features, in order of decreasing significance, were: (i) expression by large atypical cells (LACs) of CD45R0, CD43 and CD45 in pPTCLs, and of CD30 and CD15 in MCHD; (ii) means and standard deviations (SDs) of LAC nuclear-profile areas (greater in MCHD than in pPTCLs); (iii) expression of CD3 by LACs in pPTCLs; (iv) prominence of small lymphoid cells in MCHD; (v) higher percentage of medium-sized lymphoid cells in pPTCLs; and (vi) higher SDs of nuclear-profile circularity factor of small lymphoid cells in MCHD. The medians of the largest nucleolar profile areas in LACs per field did not differ in pPTCLs and MCHD, but dispersion of individual values towards higher levels was significantly greater in the latter. Stepwise discriminant analysis of test point and nucleometric variables that best distinguished pPTCLs from MCHD revealed considerable overlaps, and questionable cases tended to be intermediate between the two. In conclusion, our results confirm and expand the notion of intra-group heterogeneity, with indistinct borders and the existence of intermediate phenotypes between these two taxonomic categories of malignant lymphomas.
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PMID:Phenotypic overlaps between pleomorphic malignant T-cell lymphomas and mixed-cellularity Hodgkin's disease. 152 9

Paraffin-embedded sections of 77 peripheral T-cell lymphomas (PTCLs) were stained with several monoclonal antibodies, including the preferential T-cell markers Leu-22 (L60[CD43]) and UCHL1 (CD45RO). The staining characteristics of L60 and UCHL1 were compared to determine the value of each in the immunophenotypic analysis of PTCLs. Lineage specificity was evaluated among 39 B-cell lymphomas and 33 cases of Hodgkin's disease (HD). L60 and/or UCHL1 stained 95% of PTCLs, whereas L60 and UCHL1 alone stained 90% and 69% of cases, respectively. L60 demonstrated significantly greater numbers of immunopositive tumor cells than UCHL1 in 37% of the PTCL cases, principally because of enhanced marking of large, neoplastic cells. UCHL1 was a better marker in only 10% of the PTCL cases. L60 stained 33% of B-cell lymphomas, usually small lymphocytic or lymphoplasmacytic types. UCHL1 stained only 8% of B-cell lymphomas, all large-cell types. L60 and UCHL1 stained Reed-Sternberg cells and variants in three cases of nodular sclerosing HD. These results suggest that both L60 and UCHL1 are useful markers of PTCLs in routinely processed tissue. L60 is a more sensitive marker of large neoplastic T-cells than UCHL1 but is less lineage-specific. These antibodies are most effective when used as part of a panel of monoclonal antibodies.
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PMID:Leu-22 (L60). A more sensitive marker than UCHL1 for peripheral T-cell lymphomas, particularly large-cell types. 182 36

We studied 110 neoplastic and reactive lymphoid proliferations with three monoclonal antibodies--CD20 (L26), CD43 (Leu22), and CD45RO (UCHL1)--on B5-fixed, paraffin-embedded tissue to evaluate the utility of this panel as an immunotypic screen of such lesions. All cases were initially immunotyped by conventional methods. Genotyping by Southern blot hybridization was also done in 54 cases. Seventy-four of 79 malignant lymphomas and both of two hairy cell leukemias were of B-cell origin; and five lymphomas were defined as T-cell lineage. Lineage assignment was identical for paraffin section immunohistology and conventional immunotyping in 73 of 76 B cell and all of five T-cell tumors. CD20 was reactive with 73 of 76 B-cell tumors. CD43 was reactive with 12 of 74 B-cell lymphomas, and CD20/CD43 coexpression was seen in 11 of these cases. CD43 and CD45RO marked all of five and three of five T-cell lymphomas, respectively. Lineage assignment was identical for paraffin immunohistology and genotyping in 48 of 50 cases with identifiable gene rearrangements. Twenty-four nonneoplastic and five Hodgkin's disease cases that were studied also showed similar immunoreactivity patterns by both paraffin and conventional immunotypic methods. This panel of three monoclonal antibodies is an efficient, cost-effective approach for immunotyping most lymphoid proliferations in paraffin sections. Nevertheless, the pathologist should always try to obtain fresh or frozen tissue to aid in resolving occasional discrepant cases, to establish clonality in morphologically ambiguous ones, and to profile prognostically important phenotypic deletions.
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PMID:Reliable and cost-effective paraffin section immunohistology of lymphoproliferative disorders. 192 55

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

The authors have examined cellular areas of lymphoma tissue in 28 cases of Hodgkin's disease (HD) or anaplastic large cell lymphoma (ALCL, 'Ki-1 cell lymphoma') to evaluate the boundaries between the two entities. Methods applied included conventional histology; test point analysis; semiautomated morphometry of nuclear profile features of Reed-Sternberg and other atypical large cells (RSALCs); and immunohistochemistry of these elements on all paraffin sections and, in 15 cases, on frozen sections. Mean nuclear profile morphotypes of RSALCs per case varied independently of immunophenotype and histologic diagnosis. Conversely, immunohistochemistry demonstrated significant, although not consistent, preferential positivities of these CD30+ elements for CD15 in HD, and for epithelial membrane antigen (EMA) and CD43 in ALCLs. In the latter, RSALCs also exhibited a tendency for CD45 and CD45RO positivity and for the expression of T-cell-associated antigens. However, there were considerable overlaps. This continuous spectrum of RSALC nuclear profile morphotypes and immunophenotypes, ranging from HD over questionable cases, intermediate between HD and ALCL, to ALCLs, was paralleled by differences in the reactive component of lymphomas. Lymphocytes and granulocytes were significantly deficient in ALCLs.
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PMID:Hodgkin's disease and CD30-positive anaplastic large cell lymphomas--a continuous spectrum of malignant disorders. A quantitative morphometric and immunohistologic study. 217 9

Diffuse large B cell lymphomas (DLBLs) represent a heterogeneous collection of aggressive non-Hodgkin's lymphomas that can arise either de novo or as a result of transformation from chronic lymphocytic leukemia, small lymphocytic lymphoma, follicular lymphomas, or lymphomas of mucosa-associated lymphoid tissue. A small percentage of DLBLs express the CD5 antigen. The majority of these cases have evolved from a pre-existing low grade non-Hodgkin's lymphoma (Richter's syndrome). However, we identified and characterized nine CD5-positive DLBLs in which the patients did not have a previous history or concomitant evidence of chronic lymphocytic leukemia, small lymphocytic lymphoma, follicular lymphoma, or mucosa-associated lymphoid tissue-associated non-Hodgkin's lymphoma, suggesting that they arose de novo. All nine cases expressed CD20 and monotypic immunoglobulin, all eight cases examined expressed CD19, CD22 and CD43, eight of the nine cases expressed HLA-DR, and two of eight cases expressed CD11c. None of the cases expressed CD3, CD10, CD11b, CD21, CD23 or CD30. CD5 expression by these cells was found to be identical to that of CD5-positive B cell chronic lymphocytic leukemia by quantitative polymerase chain reaction analysis of CD5 mRNA. These nine de novo CD5-positive DLBLs exhibited clonal immunoglobulin heavy and light chain gene rearrangements but lacked integration of the Epstein-Barr virus genome and structural alterations of the bcl-1, bcl-2, c-myc, H-ras, K-ras, and N-ras proto-oncogenes and the p53 tumor suppressor gene. However, bcl-6 proto-oncogene rearrangement, which is involved in chromosome band 3q27 aberrations, was found in four cases (44.4%). This is comparable with the frequency of bcl-6 gene rearrangement in CD5-negative DLBL. In contrast, bcl-6 gene rearrangement was absent in six cases of DLBL associated with Richter's syndrome. These findings suggest that de novo CD5-positive DLBLs are genotypically similar to CD5-negative DLBLs and may be pathogenetically distinct from the DLBLs associated with Richter's syndrome.
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PMID:De novo CD5-positive and Richter's syndrome-associated diffuse large B cell lymphomas are genotypically distinct. 754 11


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