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

Clinicopathologic analyses were performed on 11 patients with histopathologic diagnosis of Hodgkin's disease which was confirmed immunohistochemically with the use of anti-Leu M 1 which is known to be specific to Reed-Sternberg cells. Patients with clinical stage II developed infradiaphragmatic involvement after Mantle field irradiation and should have been treated with extended field irradiation or combined modality therapy because of the possibility of PSIII1. Maintenance VENP therapy seemed to sustain remission but may have caused opportunistic infections. There were no rearrangements in either immunoglobulin or T cell receptor genes studied in two patients.
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PMID:[Clinicopathologic analyses of eleven patients with Hodgkin's disease]. 279 90

Diffuse, mixed small and large cell lymphomas (DML) are a heterogeneous group of non-Hodgkin's lymphomas. There are only a few published immunophenotypic and/or genotypic studies of DML, and they include a small number of cases. It is unclear whether these neoplasms are monoclonal, oligoclonal, or perhaps of dual lineage. Using monoclonal antibodies (UCHL1, MB2, MT1, LN1, LN2, and L26) that are effective in paraffin-embedded, B5-fixed tissue, 13 cases of DML were studied. This method allowed for improved correlation between cell morphology and immunophenotype compared with frozen section immunohistology. In addition, Southern blotting/DNA hybridization was used to identify directly the lineage of the neoplastic cell population. In each case a population of large B lymphocytes was demonstrated by immunohistology. In six of the cases, a single class of immunoglobulin light chains was detected by frozen section immunohistology, cytospin immunocytology, or both supporting the hypothesis that the B lymphocytes are monoclonal. In almost all the cases (12 of 13), the small cell population consisted predominantly of T lymphocytes. Immunoglobulin gene rearrangements were detected in seven cases, but no T cell receptor gene rearrangements were detected. It was concluded that DML are monoclonal lymphomas of B cell lineage with a non-neoplastic T cell component.
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PMID:Immunophenotypic and genotypic characterization of diffuse mixed non-Hodgkin's lymphomas. 280 83

In an initial survey of 16 cases of Hodgkin's disease, tissues from one case of nodular sclerosing Hodgkin's disease, a recurrence with numerous Reed-Sternberg cells, demonstrated faint heavy- and light-chain immunoglobulin gene rearrangements. Analysis of seven additional similar cases with extremely numerous Reed-Sternberg cells revealed that six of these seven cases contained clonally rearranged heavy- or light-chain genes. In addition, the original biopsy specimen from the index case (obtained two years prior to the recurrence) had the same pattern of rearrangements of the immunoglobulin genes. In contrast, a germline configuration was observed for the beta T cell receptor gene in all cases. These cases of Hodgkin's disease were also investigated for the presence of Epstein-Barr viral (EBV) genomes by Southern and slot-blot DNA hybridization analysis. Tissues from four of the 21 case studied showed evidence of EBV DNA sequences. Uninvolved lymphoid tissue from two of the positive cases failed to demonstrate viral DNA. To assess clonality of the cells containing the EBV genomes, the tissues positive for EBV DNA were also hybridized with a restriction fragment probe for the terminal sequences of the EBV genome. By this analysis three of the four cases demonstrated a clonal population of EBV-infected cells.
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PMID:Clonal antigen receptor gene rearrangements and Epstein-Barr viral DNA in tissues of Hodgkin's disease. 284 Dec 18

Important insights into leukocyte differentiation and the cellular origins of leukemia and lymphoma have been gained through the use of monoclonal antibodies that define cell surface antigens and molecular probes that identify immunoglobulin and T cell receptor genes. Results of these studies have been combined with markers such as surface membrane and cytoplasmic immunoglobulin on B lymphocytes, sheep erythrocyte receptors on T lymphocytes, and cytochemical stains. Using all of the above markers, it is now clear that acute lymphoblastic leukemia (ALL) is heterogeneous. Furthermore, monoclonal antibodies that identify B cells, such as the anti-B1 and anti-B4 antibodies in combination with studies of immunoglobulin gene rearrangement, have demonstrated that virtually all cases of non-T-ALL are malignancies of B cell origin. At least six distinct subgroups of non-T-ALL can now be identified. T-ALL is subdivided by the anti-Leu-9, anti-Leu-1, and antibodies that separate T lymphocyte subsets into three primary subgroups. Monoclonal antibodies are also useful in the subclassification of non-Hodgkin's lymphoma, and certain distinct markers can be correlated with morphologic classification. The cellular origin of the malignant Reed-Sternberg cell in Hodgkin's disease remains uncertain. A substantial number of investigators favor a myelocyte/macrophage origin based on cytochemical staining; however, consistent reactivity with antimonocyte reagents has not been demonstrated. Although monoclonal antibodies are useful in distinguishing acute myeloid from acute lymphoid leukemias, they have less certain utility in the subclassification of acute myelogenous leukemia (AML). Attempts to subclassify AML by differentiation-associated antigens rather than by the French-American-British (FAB) classification are underway in order to document the potential prognostic utility of surface markers. Therapeutic trials using monoclonal antibodies in leukemia and lymphoma have been reported. Intravenous (IV) infusion of unlabeled antibodies is the most widely used method; transient responses have been demonstrated. Antibodies conjugated to radionuclides have been quite successful in localizing tumors of less than 1 cm in some studies. Therapy trials with antibodies conjugated to isotopes, toxins, and drugs are currently planned. Purging of autologous bone marrow with monoclonal antibodies and complement in vitro has been used in ALL and non-Hodgkin's lymphoma; preliminary data suggest that this approach may be an effective therapy and may circumvent many of the obstacles and toxicities associated with in vivo monoclonal antibody infusion.
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PMID:Immunologic classification of leukemia and lymphoma. 294 Oct 82

Lymphoepithelioid lymphoma (Lennert's lymphoma) was first described as a special variant of Hodgkin's disease. This lesion is characterized by a high percentage of epithelioid and T cells and rarely contains the classical Hodgkin's/Reed-Sternberg cells. Cytogenetic abnormalities indicate that Lennert's lymphoma is of T cell origin. In the present study, immunohistochemical investigation of four cases of Lennert's lymphoma revealed two major cell populations of T cells that predominantly express the helper-inducer phenotype and Ki-M6- and Ki-M8-positive macrophages and epithelioid cells. Double-staining experiments for the detection of cell surface antigens and the proliferation-associated antigen Ki67 showed that only the CD4-positive cells (helper-inducer T cells) were proliferating. Examination of the DNA of these Lennert's lymphoma samples also indicated that monoclonal rearrangement of the T cell receptor beta-chain genes has occurred, whereas the immunoglobulin heavy- and kappa-chain genes remained in germline configuration. Our results strongly suggest that Lennert's lymphoma is a CD4-positive T cell lymphoma.
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PMID:Lymphoepithelioid lymphoma (Lennert's lymphoma) is a monoclonal proliferation of helper/inducer T cells. 294 30

Despite intensive efforts using a wide variety of approaches, the cellular lineage and clonality of the abnormal cells of Hodgkin's disease have remained an enigma. In the present study, cell separation techniques that enriched for Reed-Sternberg cells and their variants were used to generate sufficient percentages of abnormal cells to allow detection of rearrangements in these cell fractions. DNA from the involved tissues of eight Hodgkin's disease patients was subjected to Southern blot analysis to detect rearrangements of T cell antigen receptor genes and immunoglobulin genes. Immunoglobulin gene rearrangements were found in three of five cases in which Reed-Sternberg cells and their variants were enriched by cell separation techniques to cell frequencies greater than 1%. Rearrangements of immunoglobulin heavy chain genes occurred in two cases, and a lambda light chain gene rearrangement occurred in a third case. Rearrangements were not detected in lymphocyte fractions or in unseparated cells prepared from the same tissues. The putative Hodgkin's cell line, L428, also contained rearrangements of immunoglobulin heavy and kappa and lambda light chain genes and, in addition, harbored a single T cell receptor beta gene rearrangement. These findings indicate that Reed-Sternberg cell-enriched fractions contain clonal cell populations and provide a lead, at the molecular genetic level, to a possible lymphoid derivation of the Reed-Sternberg cell.
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PMID:Rearranged antigen receptor genes in Hodgkin's disease. 295 98

Antibodies directed against the human T cell receptor or the closely associated CD3 molecule stimulate polyclonal T cell proliferation via mechanisms that mimic a primary immune response. We have investigated the requirement for IL-1 production in anti-CD3 (OKT3)-mediated mitogenesis using a Hodgkin's disease cell line (L428) as the accessory cell. L428 cells did not produce detectable IL-1 following stimulation with lipopolysaccharide or phorbol ester (PMA), nor did they transcribe detectable levels of mRNA for IL-1 alpha or beta after such treatment. Despite their inability to produce IL-1, as few as 1 X 10(4) L428 cells reconstituted the proliferative response of accessory cell-depleted T cells to anti-CD3. Although larger numbers of non-rosette-forming (E-) cells were required for maximal responsiveness to anti-CD3, the maximal degree of proliferation was higher with E- cells than with L428 cells. L428-mediated T cell proliferation did not result from residual accessory cells in the responding population or an allogeneic effect since L428 cells were also capable of providing accessory cell activity for the anti-CD3-dependent generation of IL-2 by the Jurkat T cell line. Although the mechanism by which L428 cells provide accessory functions remains incompletely characterized, the ability of anti-HLA-DR F(ab')2 fragments to completely abrogate L428 and monocyte-mediated anti-CD3 mitogenesis, despite the addition of exogenous IL-1, provides evidence for the participation HLA-DR molecules in this response. These data indicate that anti-CD3-induced proliferation of unprimed human T lymphocytes can occur independently of IL-1 production by accessory cells and may involve the participation of HLA-DR molecules.
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PMID:Interleukin-1-independent activation of human T lymphocytes stimulated by anti-CD3 and a Hodgkin's disease cell line with accessory cell activity. 297 87

A novel cell line, KM-H2, was established from the pleural effusion of a patient with Hodgkin's disease of mixed cellular type. Multiple phenotypic studies were carried out with this cell line. Acid phosphatase and nonspecific esterase activities were detected. Rosette formation with T lymphocytes and the receptors for C3b and Fc portion of IgG were positive. Among the antigens tested with a total of 22 monoclonal antibodies defining hematopoietic cell subsets or lineages, Ki-1, Leu-M1, MCS1, HLA-DR, and OKT9 antigens were found to be positive. The other antigens reportedly specific for T cells, B cells, natural killer (NK) cells, monocytes, interdigitating reticulum (IR) cells and dendritic reticulum cells were negative. These phenotypic features were identical to those of the Sternberg-Reed (SR) and Hodgkin (H) cells in the fresh materials reported by other researchers. Moreover, the KM-H2 cells and the parental pleural effusion cells shared several structural chromosome anomalies. These findings indicated that the KM-H2 cells are derived from the SR and H cells. Molecular genetic analysis of the KM-H2 cells disclosed that the human immunoglobulin JH gene was rearranged but not the JK gene, and that the human T cell receptor beta chain gene was of the germline type. Based on these properties of the KM-H2 cells, Hodgkin's disease may be derived from a cell lineage other than T cell or B cell.
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PMID:Cytochemical, immunologic, chromosomal, and molecular genetic analysis of a novel cell line derived from Hodgkin's disease. 301 43

This review presents and discusses the immunogenotypic findings in 112 cases of Hodgkin's disease (HD) and eight Hodgkin's cell lines. Clonal rearrangements of the T cell receptor gamma and beta chain, as well as immunoglobulin heavy and light chain genes, are detected in the majority of nodular sclerosis and lymphocytic depletion subtypes. Together with the recent immunophenotypic data, these findings are in favour of the view that HD is a disease of activated lymphoid cells. Further investigations will be necessary to characterize the morphology and immunophenotype of the clonally rearranged cell population which seems not to be confined to the Sternberg-Reed and Hodgkin cell in every case. Prospective clinical studies including the genotype of HD cases have to be done in order to address the question of whether or not distinctive immunogenotypic profiles correlate with the clinical course of this lymphoproliferative disorder.
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PMID:Immunogenotyping in Hodgkin's disease. 304 82

The relationship between T cell receptor (TCR) beta and gene immunoglobulin heavy chain locus was investigated in 25 cases of unselected human lymphomas as well as in normal and non-neoplastic lymphoid tissues. Hybridizing our blots with Jurkat 2, a clone specific for the beta chain gene of TCR, did not demonstrate extra bands in non-neoplastic tissues composed of 50-95% T-cells. On the contrary, rearranged bands were detected in six out of six cases of T-cell lymphomas. No TCR beta gene rearrangements were detected in 11 B-cell lymphomas, which in turn presented modification of the immunoglobulin heavy chain gene germline configuration. Our results suggest that TCR beta chain gene rearrangements are a good marker for human T-cell neoplasias in humans and complement the analysis with immunoglobulin genes probes. Eighth samples were devoid of any rearrangements: this group comprises cases of Hodgkin's disease T-lymphoblastic lymphomas in clinical remission and malignancies of unknown origin, as discussed in the text. We conclude that the analysis using DNA probes specific for TCR beta and IgH genes can be of aid to the pathologist in the diagnosis and classification of human lymphomas.
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PMID:The contribution of molecular biology in the diagnosis of human lymphomas. 309 91


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