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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gene rearrangement and monoclonality have been detected in non-Hodgkin's lymphomas (NHLs). The semi-nested polymerase chain reaction (PCR) was performed to amplify IgH and the mixed PCR to TCR gamma gene rearrangements. Monoclonal band was observed in 77% of B-cell NHLs with IgH primers and 91% of T-cell NHLs with TCR gamma primers. The results show that PCR is more valuable in determining the clonality and lineage of the tumor. Moreover, 3 cases of "borderline" lymphoid hyperplasia showed clonal bands of IgH and TCR gamma gene rearrangements and follow-up studies found that one patient died of the disease 13 months after biopsy. Presumably, gene rearrangement analysis plays a significant role in the discovery of early stage disease. In comparison with Southern blot, PCR is simple, more convenient and rapid. Furthermore, no isotope is required and can be used in paraffin embedded sections, cytologic specimens and other materials. This technique can therefore be used in daily clinical diagnosis.
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PMID:[Gene rearrangements of immunoglobulin heavy chain (IgH) and T cell receptor gamma chain (TCR gamma) in non-Hodgkin's lymphomas detected by polymerase chain reaction ]. 803 76

T-cell response against tumour-associated antigens is mediated by the TCR complex. To determine a possibly restricted TCR-V beta repertoire in reactive T-lymphocytes in Hodgkin's disease (HD), 20 cases (of which 10 were EBV-positive cases) were investigated using 14 monoclonal antibodies (MoAbs) recognizing 11 different TCR-V beta region family products and Northern blot analysis with cDNA probes specific for mRNA transcripts of 11 V beta families that were not detectable by MoAbs. Four V beta families (V beta 5, V beta 6, V beta 8, V beta 19) were investigated using both immunohistochemistry (IHC) with anti-V beta MoAbs and Northern blot analysis. Immunohistochemical and Northern blot findings were correlated with the detection of the Epstein-Barr virus (EBV) genome in Hodgkin's and Reed-Sternberg cells (H-RS). The non-neoplastic lymphocytes in HD were predominantly of T-phenotype (CD3+). Most of these cells were TCR-alpha beta+ (beta F1+) and only a few T-cells were reactive for TCR-delta 1 antibody (TCR-gamma delta+). In the majority of cases helper/inducer T-cells (CD4+) outnumbered suppressor/cytotoxic T-cells (CD8+). Labelling of these samples with the panel of 14 anti-V beta MoAbs showed that only a small percentage (0.2-5.5%) of beta F1+ lymphocytes were positive with each of these MoAbs. The proportion of these cells was comparable to that seen in normal tissues. Most TCR V beta+ cells were randomly distributed, but in virtually all cases occasional V beta+ cells pertaining to the various V beta families were seen in close contact to H-RS cells. Using total RNA extracted from malignant and normal tissues, no visible band was detected with the various V beta probes. As determined in the present study, the percentage of T-cells expressing a given V beta family must be > or = 10% to be detected with Northern blot. Thus, the percentage of V beta+ cells expressing V beta families which were explored only with Northern blot were within the same range as those of the 11 different TCR-V beta region families assessed with IHC, i.e. 1-10% of lymphoid cells. The results of the present study show that in HD there is no restricted T-cell V beta repertoire usage regardless of the detection of EBV. In addition, since the various V beta families are represented in T-cell subpopulations forming rosettes around H-RS cells, we conclude that the T-cells attracted by H-RS cells constitute a polyclonal population.
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PMID:Lack of restricted T-cell receptor beta-chain variable region (V beta) usage of reactive T-lymphocytes in Hodgkin's disease. 804 34

CD30 has been extensively studied as a cell surface marker expressed by Reed-Sternberg cells of Hodgkin's disease and other hematologic malignancies, although little is known about its expression by normal lymphoid cells. We therefore characterized the requirements for the induction of CD30 expression and identified the subsets of T cells that express CD30. CD30 is inducible on approximately 15% of normal PBMC stimulated with any of a variety of nonspecific T cell activators, including PHA, Con A, anti-T11(2) + T11(3), and anti-CD3; ionomycin alone induced lower percentages of CD30+ T cells (3 +/- 2%) compared to other stimuli. Maximal numbers of CD30+ cells were observed at 48 to 72 h of activation and the addition of rIL-2 did not affect these kinetics. However, CD30 expression was enhanced by the addition of exogenous rIL-2 to any of the stimuli tested, although rIL-2 alone did not lead to CD30 expression. The induction of CD30 during anti-CD3 mitogenesis was completely inhibitable by anti-IL-2 antibodies and partially inhibitable by rIL-4, indicating a requirement for both TCR triggering and IL-2 for its expression. Dual immunofluorescence analysis revealed that CD30+ cells were confined to CD3+ T cells that coexpressed higher levels of the p55 IL-2 receptor (CD25) than the CD30- population. Furthermore, CD30 expression was restricted to a subset of cells derived from CD45RO+ T cell precursors. Cell cycle analysis showed that CD30+ expression was not cell cycle dependent. Cross-linking of membrane CD30 induced Ca2+ in TCR+, but not TCR- Jurkat T cells. These results demonstrate that CD30 can serve as a T cell signal-transducing molecule and expressed by a unique subset of activated CD45RO+ T cells.
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PMID:CD30 is a signal-transducing molecule that defines a subset of human activated CD45RO+ T cells. 810 64

Southern blot and polymerase chain reaction (PCR) were used to analyse rearrangements of antigen receptor genes in 27 cases (fresh tissues) and 51 cases (paraffin-embedded specimens) of non-Hodgkin's lymphomas (NHL). Thirty in 31 cases of NHL detected by Southern blotting showed IgH and/or IgK and/or TCR beta gene rearrangements. Of NHL with T-cell phenotype, 12 of 14 cases presented rearrangement of TCR beta gene. All the cases of analysed B-cell lymphomas displayed rearrangements of IgH and/or IgK genes. Two cases of NHL were considered bi-genotypic. Both showed IgH and TCR beta gene rearrangements. Three cases unclassified with immunophenotyping showed IgH and/or IgK gene rearrangements. In contract to the above findings all cases of reactive lymphoid hyperplasias demonstrated a germline configuration of antigen receptor genes, PCR analysis showed that monoclonal bands were observed in 77% of B-NHLs with IgH primers and 91% of T-cell lymphomas with TCR gamma primers. Besides, 4 cases of "borderline" lymphoid hyperplasias showed clonal bands of IgH and/or TCR gene rearrangements. The results suggested that gene rearrangements of antigen receptors is one of the most sensitive and valuable clonal markers in the diagnosis of lymphomas, and an important supplement to morphological diagnosis and immunophenotyping.
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PMID:[Application of gene rearrangement analysis in the diagnosis of non-Hodgkin's lymphomas]. 811 44

A case of peripheral T-cell lymphoma (PTL) occurring in a patient with Hodgkin's disease (HD) in relapse is described. The second neoplasm developed 25 months after the diagnosis of HD. Cytogenetic analysis on the lymph node biopsy at the time of diagnosis of PTL revealed the co-existence of two distinct, abnormal cell clones. The first clone was characterized by a reciprocal translocation t(5;7)(q13;q35) involving 7q35, namely the TCR-beta gene, as expected in T-cell lymphomas. The second cell clone carried trisomies for chromosomes 2, 5, 7, and 14. By immunophenotypic and molecular analysis as well as by in situ hybridization, it was possible to prove that the malignant T-cells and the Reed-Sternberg cells corresponded to different cell clones, one carrying the structural chromosome abnormalities and one carrying the numerical chromosome anomalies. These results indicate that the present case represented a true composite lymphoma.
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PMID:T-cell lymphoma developing in Hodgkin's disease: evidence for two clones. 813 97

Analysis of complementary RNA molecules of junctional regions of rearranged T-cell-receptor-gamma genes show a pattern of conformational polymorphisms which is specific for an individual lymphocytic clone. In a blinded study we analysed formalin-fixed, paraffin-embedded histological specimens from gastrointestinal lymphomas and control tissues (lymphomas: pleomorphic T-cell 10, anaplastic large cell [Ki1+] 9, centroblastic 5, immunocytoma 1, B-CLL 2, Hodgkin's 2, centroblastic-centrocytic 1, MALT [mucosa associated lymphoid tissue] 1, T-cell acute lymphoblastic leukaemia 1, non-lymphoid or polyclonal lymphoid tissues 5). Junctional regions of rearranged TCR-gamma genes were amplified by the polymerase chain reaction and the products were transcribed into cRNA. Conformational patterns of cRNA molecules were analysed by polyacrylamide gel electrophoresis. 13/20 T-lineage lymphomas and the T-cell acute lymphocytic leukaemia displayed a distinct cRNA band pattern, all B-lineage lymphomas and the non-lymphoid control tissues were negative. Only one case of nasopharyngeal (lymphoepithelial, Schmincke-Regaud) carcinoma showed a faint cRNA banding pattern. This novel and non-radioactive assay allows for the rapid detection and molecular characterization of clonal lymphoid populations in minute histological biopsy specimens.
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PMID:Detection of clonal T-cell populations in gastrointestinal lymphomas by analysis of cRNA conformational polymorphisms of rearranged T-cell-receptor-gamma genes. 819 20

In this study we show that in vitro cultured human polyclonal NK cell lines and clones express the Ki-1/CD30 Hodgkin-associated antigen, identified by the BER-H2 monoclonal antibody. The percentage of BER-H2+ cells ranged from 19% to 67% in five polyclonal NK cell lines and was 31% and 20% in two NK clones. The intensity of BER-H2 mAb staining on cultured NK cells was remarkably lower than that found on the L540 Hodgkin's lymphoma cell line. Resting PBL populations that had been enriched for NK cells failed to react with the BER-H2 mAb. Western blot analysis performed on cell lysates from a polyclonal NK cell line and from the NK3.3 NK-like cell line revealed that BER-H2-reactive molecules consisted of two major bands of approximately 110 kD and 100 kD. Two bands displaying an identical electrophoretic mobility were also found in lysates of the L540 cell line. The BER-H2 mAb failed to inhibit the nonspecific activated killer activity of cultured NK cells against both K562 and MeWo tumour target cells. In addition, the BER-H2 mAb was unable to trigger the cytolytic activity of NK cells in a redirected killing assay. The observation that cultured human NK cells express the Ki-1/CD30 antigen may be of relevance for the possible lineage assignment of K11/CD30+ lymphoid cell neoplasia with unrearranged TCR genes.
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PMID:Cultured human NK cells express the Ki-1/CD30 antigen. 828 Jun

Nineteen patients with Hodgkin's disease (HD), representing 4 different subtypes, were examined for immunophenotype and immunogenotype. Quantitative immunophenotypic analysis of 13 cases revealed a predominance of Leu1 and Leu3 T cells in all subtypes, except in the case of HD lymphocytic-depression (HDLD). The positive rate of LeuM1 and Ki1 in Reed-Sternberg (RS) cells was 65% (11/17) and 73% (11/15), respectively. In DNA hybridization analysis, 5 of the 19 cases of HD were found to have gene rearrangements--immunoglobulin (Ig) gene rearrangements in 3 cases and T cell receptor beta chain (TCR beta) gene rearrangements in 2 cases. Epstein-Barr (EBV) DNA genomes were detected in 8 cases, including 2 of 5 cases which previously had been shown to contain clonal Ig and TCR beta gene rearrangements. By contrast, there were no detectable cytomegalovirus (CMV) DNA sequences in 19 cases of HD or 30 cases of non-Hodgkin's lymphoma (NHL). Although our findings differed somewhat from those obtained on Westerners, they suggest the presence of a monoclonal lymphoid population in HD patients and that the EBV is related to the etiology of HD.
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PMID:Immunoglobulin and T cell receptor beta chain gene rearrangements and Epstein-Barr viral DNA in tissues of Hodgkin's disease in Taiwan. 839 9

We have examined the production of interferon (IFN) gamma by peripheral blood mononuclear cells (PBMC) in 22 patients with Hodgkin's disease (HD) in active phase of the disease, 12 patients in clinical remission and 16 healthy subjects. The level of IFN gamma in supernatants of PBMC stimulated for 72 h with anti-CD3 monoclonal antibody (mAb), measured by sandwich enzyme immunoassay (ELISA) was 50.4 +/- 2.3 U/ml in active phase; 137.0 +/- 7.4 U/ml in clinical remission patients; and 520.0 +/- 10.0 U/ml in the controls; the difference between the groups was statistically significant. Co-stimulation with interleukin-2 (rIL-2) markedly amplified production of IFN gamma. The mean levels were 220.8 +/- 7.0 U/ml, 590.7 +/- 3.6 U/ml and 2111.1 +/- 17.3 U/ml in active phase HD, clinical remission and controls, respectively, the difference between groups was statistically significant. The patients showed the same kinetic pattern as healthy individuals. Our results indicate that patients with HD have severely impaired TCR/CD3 activation pathway resulting in significantly depressed IFN gamma response to anti-CD3 mAb and anti-CD3 + rIL-2 in vitro stimulation and provide support for the possible clinical use of IFN gamma as an immunopotentiating agent in patients with HD.
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PMID:Decreased production of interferon gamma by anti-CD3 monoclonal antibody and interleukin-2-stimulated peripheral blood mononuclear cells in Hodgkin's disease. 855 74

T-cell Non-Hodgkin's lymphomas (T-NHL) can be defined as clonal malignant proliferations related phenotypically and functionally to normal T-cell populations of the lymphoid tissue. There is increasing evidence that T-NHL with similar morphology but originating from different sites differ in their clinical behaviour, immunophenotypic features, oncogene expression and relation with oncogenic viruses such as HTLV-I and EBV. Indeed, it has been shown that the prevalence of EBV in T-NHL is related to the site of origin. Thus, EBV was found in nearly all nasal T-NHL but only in a proportion of primary nodal, lung, gastrointestinal and Waldeyer's ring T-NHL while it was undetectable in most primary cutaneous T-NHL. Besides their constant association with EBV, nasal T-NHL display peculiar clinical, histological, immunophenotypic and genotypic features. They present clinically as lethal midline granuloma and histologically as pleomorphic malignant tumours variably associated with angiocentricity, angioinvasion and necrosis. Moreover, they frequently exhibit extensive loss of T-cell antigens, including CD3 and TCR alpha beta and gamma delta proteins, usually express the Natural Killer (NK)-related CD56 antigen and frequently show absence of clonal rearrangements of TCR beta, gamma and delta loci. Therefore, among T-NHL, nasal T-NHL can be regarded as a distinct clinicopathologic entity associated with EBV, which could be derived either from immature T-cells or from NK cells.
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PMID:Epstein-Barr virus (EBV) in extranodal T-cell non-Hodgkin's lymphomas (T-NHL). Identification of nasal T-NHL as a distinct clinicopathological entity associated with EBV. 858 Aug 26


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