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)

Lymph nodes were examined from four patients with incipient adult T-cell leukemia-lymphoma (ATLL) who had mild lymphadenopathy, fatigue, no or a few atypical lymphocytes in their peripheral blood, and integrated proviral human T-cell lymphotrophic virus type I (HTLV-I) DNA in the nodes. The HTLV-I DNA was detected by southern blot analysis and/or polymerase chain reaction in the lymph nodes of all cases. The nodal architecture was preserved. Some scattered or aggregated highly lobular, cerebriform, or Reed-Sternberg-like giant cells were observed, with occasional mitoses and diffuse infiltration of small to medium-sized lymphocytes, with no or minimal nuclear abnormalities in the enlarged paracortex. The giant cells were usually positive for Ki-1 and also for UCHL-1 and other T-cell markers but negative for Ber-H2. Rearrangement and/or deletion of T-cell receptors were found in three of four patients. All patients died within 2 years, with transformation to overt leukemia-lymphoma occurring in three patients, and pulmonary carcinoma in one. The incipient or prelymphomatous phase of ATLL should be differentiated from Hodgkin's disease because of the distinctly different prognoses of these two diseases.
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PMID:Lymph nodes in incipient adult T-cell leukemia-lymphoma with Hodgkin's disease-like histologic features. 200 51

We have examined 165 unselected cases of non-Hodgkin's lymphomas for rearrangements involving the t(14;18) major breakpoint region using a polymerase chain reaction (PCR) and direct sequencing of amplified major breakpoint region bcl-2/JH junctional regions. The lymphomas, diagnosed according to the updated Kiel classification, consisted of 33 centroblastic-centrocytic, 37 centroblastic, 27 immunocytic, 10 immunoblastic, 10 centrocytic, 2 lymphoblastic, 2 Ki-1-positive anaplastic large cell, 14 peripheral T-cell, and 4 unclassified lymphomas. In addition 18 chronic lymphocytic leukemias, 2 hairy cell leukemias, and 6 plasmacytomas were studied. In 17 cases a bcl-2/JH gene fusion sequence was amplified by PCR. A bcl-2/JH gene fusion was detected only in three lymphoma subgroups: 13 of 33 centroblastic-centrocytic (39%), 2 of 37 centroblastic (6%), and 2 of 27 immunocytic (8%) were positive. In two cases, major breakpoint region bcl-2 rearrangements verified by genomic Southern analysis were not detected by PCR. Direct sequencing of all 17 PCR-amplified, previously uncharacterized t(14;18) junctional regions provided corroborating evidence for the specificity of the assay. The procedure gave sequencing results even from limited amounts of lymphoma cells as obtained by fine needle aspiration of lymph nodes or from clinically uninvolved sites. Clone-specific sequences were identified due to the involvement of different JH segments, the variations among the exact JH and bcl-2 breakpoint positions, and the extensive incorporation of junctional region (D-) N-nucleotides. These clone-specific sequences allow accurate identification of clinically occult lymphoma cells and reduce the threat of false positive results. The finding of exceptionally long intervening sequences in some of the junctions and the partial homology with published DH segments in three cases support the view that some of the putative N-regions harbor DH regions.
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PMID:Frequency and structure of t(14;18) major breakpoint regions in non-Hodgkin's lymphomas typed according to the Kiel classification: analysis by direct DNA sequencing. 203 99

The clinical, prognostic, phenotypic, and genotypic findings of 30 patients with large cell anaplastic lymphoma (Ki-1-positive large cell lymphoma) were analyzed. There were 13 male and 17 female patients (male-female ratio, 0.8) whose ages ranged from 3 to 81 years of age (mean, 28 years of age; 67% of the patients younger than 30 years of age). The 5-year survival rate was 52%; this was better than that of other types of high-grade peripheral T-cell lymphoma. Histologic examination showed distinctive morphologic features such as tumor cell pleomorphism, sinus infiltration, fibrosis, partial lymph node involvement, sparing of B-cell regions, and occasional plasma cell infiltrates. Eighty percent of the cases were of T-cell phenotype, and others expressed neither B-cell nor T-cell markers. The tumors were frequently positive for a histocompatibility antigen (HLA-DR), CD25 (the interleukin-2 receptor), and epithelial membrane antigen. Rearrangements of the T-cell receptor beta gene were observed in nine of 13 cases (69%). These findings indicated that many of the tumors had the phenotype and genotype of activated T-cells. This study also showed that large cell anaplastic lymphoma has a survival figure intermediate between Hodgkin's disease and low-grade peripheral T-cell lymphoma.
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PMID:Clinicopathologic study of large cell anaplastic lymphoma (Ki-1-positive large cell lymphoma) among the Japanese. 204 32

Five monoclonal CD30 antibodies and two Fab' fragments were linked to deglycosylated ricin A chain (dgA), and their potential as immunotoxins for the treatment of Hodgkin's disease was evaluated. Cross-blocking experiments demonstrated that HRS-1, HRS-3, HRS-4, and Ber-H2 recognize the same epitope on the CD30 antigen and that Ki-1 binds to a different epitope. Scatchard analyses showed that HRS-3, HRS-4, and Ber-H2 bound strongly to L540 Hodgkin cells (Kd 15, 7, and 14 nM, respectively), whereas HRS-1 and Ki-1 bound more weakly (Kd 160 and 380 nM, respectively). The different affinities of the antibodies correlated closely with their cytotoxic potency as immunotoxins. HRS-3.dgA, HRS-4.dgA, and Ber-H2.dgA inhibited the protein synthesis of L540 cells by 50% at concentrations of 0.9-2.0 x 10(-10) M, whereas HRS-1.dgA and Ki-1.dgA were about 100 times less potent with 50% inhibitory concentrations of 0.8-1.0 x 10(-8) M. The most effective immunotoxins, HRS-3.dgA and HRS-4.dgA, were only 15 times less toxic than ricin itself. HRS-3 Fab'.dgA and HRS-4 Fab'.dgA were 7.8 and 3 times less potent than their IgG.dgA counterparts with 50% inhibitory concentrations of 7 x 10(-10) and 3 x 10(-10) M, respectively. Staining of human tissues revealed an unexpected cross-reactivity of HRS-4 with pancreatic cells of malignant and nonmalignant origin. HRS-1, HRS-3, Ber-H2, and Ki-1 showed very little cross-reactivity with any normal human tissues. It is concluded that HRS-3.dgA and HRS-3 Fab'.dgA are the immunotoxins of choice for in vivo therapy.
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PMID:Evaluation of ricin A chain-containing immunotoxins directed against the CD30 antigen as potential reagents for the treatment of Hodgkin's disease. 215 74

The authors studied four cases of diffuse, large cell non-Hodgkin's lymphomas with strong Ki-1 expression to determine if they shared characteristic ultrastructural or morphometric features in common. The tumor cells in these lymphomas all had very abundant cytoplasm, which often showed a concentration of organelles, especially mitochondria and Golgi apparatus, in regions next to nuclear concavities. One case had very complex cytoplasmic membrane projections resembling a "microvillous" lymphoma. These ultrastructural features combined with the frequent reniform nuclei and scattered lysosomes suggested histiocyte differentiation. However the immunophenotype was variable, more often showing "activation" markers and abnormal T-cell marker patterns. The mean nuclear area for all cases was between 38.3 +/- 12.7 to 42.3 +/- 16.2 microns2, roughly twice the size of the small lymphocyte population. The nuclear contour index, a measure of irregularity of the nuclear membrane, ranged from 4.75 +/- 0.86 to 6.36 +/- 1.89 (a circle is 3.54). These nuclear parameters are comparable in size to those of previously measured large cell lymphomas but exhibit more nuclear irregularity than most. Ki-1 lymphomas appear to represent a somewhat diverse group of tumors of lymphoid origin that exhibit some hybrid features of histiocytes.
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PMID:Ki-1-positive non-Hodgkin's lymphomas. An immunophenotypic, ultrastructural, and morphometric study. 215 26

The clinical, histological, immunophenotypic and genotypic properties of four cases of lymphoma of true histiocytic origin are described. The cases were identified by typing 925 non-Hodgkin's lymphomas by immunophenotypic and/or genotypic techniques, and they all presented with skin lesions. The histological and immunophenotypic examination showed dense, diffuse infiltrates of markedly pleomorphic mononuclear cells that were positive for macrophage-associated markers, and negative for B-cell, T-cell and myeloid cell-associated antigens. Staining for Ki-1 and epithelial membrane antigen was also negative. Gene rearrangements studies were performed in three cases, and all of these showed germline configuration of both T-cell receptor and immunoglobulin genes. In all cases, the clinical course was aggressive with rapid and widespread dissemination to internal organs, poor response to conventional chemotherapy, and short survival times (0.5 to 14 months). This suggests that although true histiocytic tumours are very rare, their recognition may be important for clinical and/or prognostic reasons.
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PMID:Malignant lymphomas of true histiocytic origin. A clinical, histological, immunophenotypic and genotypic study. 215 39

Lymph nodes from patients with acute infectious mononucleosis (AIM) typically show marked paracortical expansion and a prominent immunoblastic proliferation that can occur in nodules and sheets, as well as within sinuses. The marked immunoblastic proliferation, coupled with Reed-Sternberg-like cells and a polymorphous inflammatory cell background, may simulate either non-Hodgkin's lymphoma or Hodgkin's disease. A recently described entity, Ki-1-positive lymphoma, or large cell anaplastic lymphoma, shares some clinicopathologic and phenotypic features with AIM and must be considered in the differential diagnosis. The present case describes a 20-year-old male who had signs and symptoms consistent with AIM, which he was later proven serologically to have, but whose cervical lymph node showed features suspicious for large cell anaplastic lymphoma. In addition, the Ki-1 (CD30) antigen was expressed by some of the atypical immunoblasts, further raising this possibility.
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PMID:Acute infectious mononucleosis. CD30 (Ki-1) antigen expression and histologic correlations. 184 59

The Hodgkin-associated Ki-1 antigen (CD30) consists of a 120-kDa membrane-associated glycosylated phosphoprotein (Ki-1/120) and a 57-kDa non-glycosylated phosphoprotein (Ki-1/57) which only occurs intracellularly. Both molecules are phosphorylated at serine residues. An analysis of the peptide fragments resulting from staphylococcal V8-protease digestion of the Ki-1/57 molecule revealed identical bands irrespective of the cell source. Only a few bands of the Ki-1/57 digests appeared among the peptide fragments of the Ki-1/120 membrane antigen. The protein kinase activity was tested for both forms of the Ki-1 antigen. The Ki-1/120, devoid of the Ki-1/57 molecule, was immunoprecipitated from cell lysates of Hodgkin-analogous cell lines L428 or L540, which had been loaded with the Ki-1 or the Ki-1-analogous antibodies Ber-H2, HSR-1, -2 and -3 (method 1). These other antibodies reacted with the Ki-1/120, but not with the Ki-1/57 antigen. The latter, devoid of the Ki-1/120, was isolated from L540 cells after removal of the membrane form by method 1 or from U266/Bl myeloma or Raji Burkitt lymphoma cells which only contain the smaller form. Effects of non-specific adsorption were eliminated by various control precipitates. The Ki-1/57 intracellular antigen showed autophosphorylation and could phosphorylate histones as well. In contrast, a protein kinase activity of the membrane-associated Ki-1/120 could not be demonstrated.
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PMID:Protein kinase activity of the intracellular but not of the membrane-associated form of the Ki-1 antigen (CD30). 216 Nov 15

The expression of T-cell receptors (TCR) in malignant lymphomas was examined immunohistochemically by monoclonal antibodies which react with the TCR beta or TCR delta chain. TCR beta was expressed in 16 out of 47 non-Hodgkin's lymphomas. These included 15 T-cell lymphomas and 1 Ki-1 lymphoma. The anti-TCR beta chain antibody, beta F1, did not react with 26 B-cell lymphomas, 1 Ki-1 lymphoma or 6 Hodgkin's disease. This anti-TCR delta chain antibody, TCR delta 1, did not react with any type of malignant lymphoma. Although TCR beta and CD3 were co-expressed in normal lymphoid tissues and most T-cell lymphomas, 3 cases of CD3+ CD4+ CD8- T-cell lymphoma failed to express TCR beta. TCR beta and Ig JH gene configurations in malignant lymphomas were examined by Southern hybridization. Although each of 9 T-cell lymphomas had a rearranged TCR beta locus, TCR beta gene rearrangement in the 3 cases of beta F1- CD3+ T-cell lymphomas was demonstrated by Southern blot. No transcripts of the TCR beta gene could be found in 2 out of the 3 beta F1- CD3+ T-cell lymphomas by Northern blot, indicating the lack of TCR beta protein expression to be due to non-transcription of the TCR gene. Loss of TCR beta proteins in these T-cell lymphomas is thus quite likely to be associated with T-cell tumour activation and progression, since 3 beta F1- CD3+ T-cell lymphomas expressed CD25 (interleukin-2 receptor) to a high degree.
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PMID:Relationships among expression, transcription and rearrangement of T-cell receptor beta gene in T-cell lymphomas. 216 38

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


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