Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lymphomatoid papulosis is a distinct entity in which recurring crops of haemorragic and necrotic papules display a cytologically malignant infiltrate. The aberrent cell is now generally accepted to be an active T helper phenotype. The expression of Ki-1 (CD30) on a significant portion of the infiltrating cells characterizes lymphomatoid papulosis and relates this disorder with Hodgkin's disease, mycosis fungoides and anaplasic T cell lymphoma which may be associated in 10 to 20% of lymphomatoid papulosis. The categorization of this disease as a benign disorder versus lymphoma remains controversial. Studies of T cell receptor gene rearrangement demonstrate clonality in many cases. So, this monoclonal population could have a malignant transformation induced by a triggering stimulus such as genetic translocation, or viral infection. Finally, recent opinions consider that lymphomatoid papulosis and Ki-1 (CD30) lymphomas are different parts of a clinical and histological spectrum constituted by cutaneous Ki-1 lymphoid infiltrates.
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PMID:[Lymphomatoid papulosis]. 756 10

We describe a modified denaturing gradient gel electrophoresis (DGGE) procedure with a 40-nucleotide GC clamp in the polymerase chain reaction to improve resolution in amplifying T cell receptor-gamma (TCR-gamma) rearrangements. DNA from 46 cases of lymphoblastic leukemia/lymphoma, 5T cell lines, 2 B cell lines, 7 normal lymphocytes, and 3 cases of Hodgkin's disease was amplified by polymerase chain reaction. In addition, 20 cases of paraffin-embedded T cell lymphomas and 5 cases of reactive hyperplasia were also studied. Clonal TCR-gamma rearrangements were identified on DGGE by the presence of a predominant band. Results obtained from 5 T cell lines and 12 lymphoblastic leukemia/lymphomas containing known TCR-gamma gene rearrangements revealed 100% concordance in detecting clonal rearrangements between DGGE and traditional Southern blot analysis. Of the remaining 34 lymphoblastic leukemia/lymphoma cases studied by DGGE alone, 30 were positive. DGGE analysis of 10 lymphoblastic leukemia/lymphoma cases with known group IV gamma to J gamma 1 or J gamma 2 rearrangement sequences confirmed that the electrophoretic migration was dependent on the tumor-specific rearranged TCR-gamma sequence. In addition, 17 of 20 cases of paraffin-embedded T cell lymphomas were positive by DGGE, 6 of which had the clonal population also identified in fresh tissue DNA. DGGE analysis of GC-clamped polymerase chain reaction products can provide a way to more accurately detect TCR-gamma clonality of lymphoid tumors and can be applied to archival tissues.
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PMID:Analysis of T cell receptor-gamma gene rearrangements by denaturing gradient gel electrophoresis of GC-clamped polymerase chain reaction products. Correlation with tumor-specific sequences. 785 38

Fifty patients with various hyperplastic and malignant lymphoproliferative diseases were investigated for evidence of human herpesvirus-6 infection. Virus DNA and antigen expression was investigated in lymph node biopsies by in situ hybridization and immunohistology and was correlated with data of immunophenotyping. Supplemental immunoglobulin- and T cell receptor gene rearrangement studies were used to support the classification of the proliferative lymphoid lesion. Elevated numbers of cells carrying HHV-6 DNA and/or antigens were found in cases of Hodgkin's lymphoma and follicular center cell non-Hodgkin's lymphoma as well as atypical polyclonal lymphoproliferation (APL), yet not in reactive lymphoid hyperplasia and in most other lymphomas. Immunophenotyping showed that virus -infected cells were primarily lympho-histiocytic elements, less frequently Hodgkin's- and Reed-Sternberg cells, and not malignant B lymphocytes as in follicular center cell lymphomas. This suggests that the virus is rather not the causative oncogen in these cases, yet does not exclude a cocarcinogenic effect of it during the development and ths course of uncontrolled lymphoproliferation.
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PMID:Semi-quantitative in situ hybridization and immunohistology for antigen expression of human herpesvirus-6 in various lymphoproliferative diseases. 789 78

Antigen recognition by T cells is determined by an antigen specific T cell receptor (TCR). Two heterodimeric TCR structures associated with CD3 have been defined: TCR alpha beta and TCR gamma delta. TCR alpha beta and its function are well described but the role of TCR gamma delta in normal and lymphoproliferative disorders is not well established. In newly diagnosed or relapsed/refractory Hodgkin's disease (HD), a disease associated with defective T cell functions and increased sIL-2R, we determined levels of seven TCR alpha beta variable regions [beta V5(a), beta V5(b), beta V6(a), beta V12(a), alpha beta V(a), alpha V2(a)] and TCR gamma delta by using monoclonal antibodies (MCA). TCR gamma delta levels did not show any difference, but several variable regions of the TCR alpha beta differed when groups are compared with each other and the control group.
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PMID:Peripheral T cell receptors alpha beta and gamma delta in patients with Hodgkin's lymphoma. 799 94

The use of molecular methods to diagnose malignant lymphoma, while firmly established in reference centers, has not been well evaluated at the community level. A group of 57 specimens from patients with non-Hodgkin's lymphomas (NHL), lymphoid leukemias (LL), and a variety of other lymphoproliferative lesions with the Southern blot methodology have been studied by us. Molecular probes to the joining regions of the heavy (JH) and light (J kappa) immunoglobulin chains and the beta (J beta 1-2) chain of the T cell receptor genes were used. Gene rearrangements were detected in 90 percent of all NHL/LL with a 95 percent detection rate specifically for B-NHL/LL. In comparison, phenotypic analysis by immunoperoxidase stains favored a B phenotype in 75 percent of those cases, while flow cytometry assigned 63 percent of cases to a B cell lineage. Gene rearrangements were detected in four of six cases of T-NHL for a rate of 67 percent. The six other lymphoproliferative lesions included Hodgkin's disease, Castleman's disease, and a case of lymphoid hyperplasia. No rearrangements were detected in these specimens. The studies allowed development of increased confidence in the diagnosis of NHL/LL on ever smaller specimens. The availability of these studies has also helped establish a priority of handling all specimens so that the most appropriate studies can be performed to yield the most useful diagnostic information.
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PMID:Gene rearrangements in malignant lymphomas. 804 94

Tumor immunotherapy should increase both the number of T cells that kill the tumor and the likelihood that those cells are activated at the tumor site. Bispecific monoclonal antibodies (Bi-mAbs) were designed that bound to a Hodgkin's tumor-associated antigen (CD30) on the tumor and to either CD3 or CD28 on the T cell. Immunodeficient mice were cured of established human tumors when mice were treated with both the CD3-CD30 and the CD28-CD30 Bi-mAbs and then given human peripheral blood lymphocytes that had been incubated with the CD3-CD30 Bi-mAb and cells that expressed CD30. The enrichment of human T cells within the tumor and the fact that established tumors can be cured may indicate in situ activation of both the T cell receptor and the costimulatory pathway.
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PMID:Cure of xenografted human tumors by bispecific monoclonal antibodies and human T cells. 817 37

A novel Hodgkin cell line, designated HD-MyZ, was established from the pleural effusion of a 29-yr-old patient with Hodgkin's disease (HD) of nodular sclerosing type. The majority of cells grow adherently and display typical morphological characteristics of Reed-Sternberg (RS) and Hodgkin (H) cells, i.e., large multi- and mononucleated cells with prominent nucleoli. Immunofluorescence analysis revealed a myelomonocytoid immunophenotype (expression of CD13 and CD68, and lack of lymphoid markers). HD-MyZ cells strongly expressed restin, a recently described intermediate filament-associated protein, the expression of which is restricted to H cells, RS cells, and in vitro cultivated peripheral blood monocytes. In addition mRNA expression of c-fms (colony-stimulating factor 1 receptor) could be induced in HD-MyZ cells by phorbol myristate acetate (PMA) stimulation. Southern blot analysis did not detect rearrangement of T cell receptor beta and immunoglobulin H loci, thus demonstrating the lack of lymphoid commitment. HD-MyZ cells were also devoid of Epstein-Barr virus genomes. HD-MyZ cells constitutively express mRNAs for interleukin 1 alpha (IL-1 alpha), IL-1 beta, IL-5, IL-6, IL-7, IL-8, IL-10, IL-1 receptor (type I), and IL-6 receptor. Stimulation of cells with PMA increased mRNA expression as well as the secretion of IL-1 beta, IL-6, and IL-8, and induced the de novo expression of IL-8 receptors. Xenotransplantation into severe combined immunodeficient (SCID) mice by intravenous or subcutaneous inoculation led to development of disseminated tumors with infiltrative and destructive growth. In addition lymphadenopathy, pleural effusion, and infiltration of spleen were observed. Morphological and immunological analysis of tumor cells revealed the same features as HD-MyZ cells. This cell line might be an important tool for understanding the pathogenesis and biology of HD. In addition the SCID mice model might prove helpful in developing new therapeutic strategies.
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PMID:Characterization of a novel Hodgkin cell line, HD-MyZ, with myelomonocytic features mimicking Hodgkin's disease in severe combined immunodeficient mice. 838 41

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

CD30 is a member of the tumor necrosis factor superfamily and a surface marker for Hodgkin's disease. Normal activated T cells and several virally transformed T or B cell lines also show CD30 expression. The interaction of CD30 with its ligand induces cell death or proliferation, depending on the cell type. In this report we characterize the signals mediated by the intracellular domain of CD30 and show that, in combination with signal(s) transduced by the T cell receptor, the multimerization of CD30 cytoplasmic domain induces Fas(CD95)-independent cell death in T cell hybridomas. Deletion analysis shows that the COOH-terminal 66 amino acids of CD30 are required to induce cell death. Using the yeast two-hybrid system, we have identified that the same region of CD30 interacts with tumor necrosis factor receptor-associated factor (TRAF)1 and TRAF2. These results indicate that TRAF1 and/or TRAF2 play an important role in cell death in addition to their previously identified roles in cell proliferation.
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PMID:T cell receptor-dependent cell death of T cell hybridomas mediated by the CD30 cytoplasmic domain in association with tumor necrosis factor receptor-associated factors. 862 80

Based on the presence of T cell receptor-beta (TcR-beta) gene rearrangements in L428 and HDLM-1 cells, the expression of CD2 in HDLM-1 cells, and the presence of immunoglobulin heavy-chain (IgH) gene rearrangement in KM-H2 cells, some researchers have concluded that these long-term cell lines derived from patients with Hodgkin's disease are lymphoid in nature. The information obtained from these cell lines has also been used in arguments for a lymphoid origin of H-RS cells in tissue despite the frequent absence of lymphoid markers and Ig/TcR gene rearrangements in these cells. We questioned whether one can use the limited expression of lymphoid markers or the limited gene rearrangement to conclude that H-RS cells have a lymphoid origin, because these markers may be aberrant in tumor cells. In this study, we examined the expression of two T-cell-specific transcription factors (TCF-1 and GATA-3) and one B-cell-specific transcription factor (BSAP) in cultured H-RS cells by using a gel mobility shift assay. The sensitivity and specificity of this assay for determination of cell lineage have been established in a large number of cultured human and murine cell lines. All three types of H-RS cell lines were consistently negative for BSAP, TCF-1, and GATA-3. The absence of GATA-3 was confirmed in H-RS cells in tissues by an in situ hybridization technique. Virtually all B-cell lines, with the exception of some myeloma cell lines, are positive for BSAP, which is the transcription factor for promoters for several B-cell markers, including VpreB1, lambda 5, CD19, and CD20. All T-cell lines tested were positive for TCF-1 and GATA-3, which are the transcription factors for promoters for several T-cell-restricted markers, including CD2, CD3, TcR, and lck. The absence of BSAP, TCF-1, and GATA-3 clearly indicates an underlying difference between H-RS cells and lymphoid cells.
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PMID:Absence of T-cell- and B-cell-specific transcription factors TCF-1, GATA-3, and BSAP in Hodgkin's Reed-Sternberg cells. 878 Jan 59


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