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)

T-cell lymphomas with similar morphology but with different sites of origin have a different clinical behavior. The theoretical explanation for this finding originates from the hypothesis that non-Hodgkin's lymphomas (NHLs) are neoplastic equivalents of immunological reactions involving tissue-restricted lymphocytes. This hypothesis also implies that T-NHLs originating from different sites differ in their genesis, and thus may differ in oncogen expression, expression of adhesion molecules, or presence of certain DNA/RNA viral sequences. Therefore, we have investigated in T-cell lymphomas with similar morphology originating from different sites, ie, nose (n = 5; all pleomorphic small- or medium- and large-cell T-cell lymphomas [PTL]), skin (PTL, n = 6; anaplastic large-cell [ALCL], n = 11), gut (PTL, n = 8; ALCL, n = 4), and lung (PTL, n = 6), the presence of Epstein-Barr virus (EBV) at the DNA, RNA (EBER 1 and EBER 2), and protein level (LMP-1). A double-staining technique was used to detect EBER 1/2, LMP-1, and differentiation markers at the single-cell level. High numbers of EBER 1/2-positive tumor cells (> 100 per medium power field [mpf]) were found in five of five nasal T-cell lymphomas, none of 17 primary cutaneous T-cell lymphomas, one of 12 gastrointestinal T-cell lymphomas (ALCL), and two of six pulmonary T-cell lymphomas. These lymphomas are therefore called EBV-associated lymphomas. In contrast to our earlier findings in lymph nodes, no extranodal lymphomas were found, with only a few EBV-positive tumor cells. Five gastrointestinal cases positive for EBV by polymerase chain reaction (PCR) showed that EBER 1/2 was only found in sporadic nonneoplastic, ie, reactive lymphocytes. Angiocentricity was present in 18 PTL and one ALCL, but not associated with the presence of EBV. These results indicate that the presence of EBV in extranodal T-cell lymphomas is site-restricted and argues for a different pathogenesis of T-cell lymphomas with similar morphology but originating from different sites. The presence of EBV in most tumor cells in these EBV-associated lymphomas suggests that when present, EBV might be important in the pathogenesis of these lymphomas.
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PMID:Presence of Epstein-Barr virus in extranodal T-cell lymphomas: differences in relation to site. 812 52

The authors studied five patients with primary cutaneous Hodgkin's disease (PCHD). Each patient presented with skin lesions without evidence of systemic HD. Skin lesions were papules or nodules, many of which regressed spontaneously. Lesions were distinguished from lymphomatoid papulosis (LyP) by the presence of numerous diagnostic Reed-Sternberg (RS) cells that expressed CD30 and CD15 but were negative for CD45R; LyP lesions usually are CD15-, CD45R+. Anaplastic large cell lymphoma (ALCL) was excluded by the polymorphous background of inflammatory cells in PCHD. Three patients with PCHD had a benign course without systemic disease with up to 20 years of follow-up, whereas two other patients developed mixed-cellularity HD in lymph nodes 2 months and 6 years following the onset of PCHD. This study indicates that PCHD does occur as a rare but distinct clinicopathologic entity morphologically and immunophenotypically indistinguishable from nodal HD but with an unexpectedly indolent course in some patients. Patients with PCHD should be observed for development of systemic HD, but unlike patients with LyP or ALCL, an association of PCHD with mycosis fungoides or cutaneous T-cell lymphoma has not yet been observed.
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PMID:Primary cutaneous Hodgkin's disease. Unique clinical, morphologic, and immunophenotypic findings. 816 Sep 26

We recently characterized a novel putative intermediate-filament associated protein which is strongly expressed in the Reed-Sternberg cells of Hodgkin's disease. Therefore we named the protein 'restin', an acronym for Reed-Sternberg cell intermediate filament-associated protein. The protein is also expressed in anaplastic large cell lymphoma or Ki-1 lymphoma, a non-Hodgkin's lymphoma phenotypically related to Hodgkin's disease. Although the functions of restin are not yet fully elucidated, transfection experiments demonstrate that overexpression of the protein increases cell growth by a mechanism which may involve upregulation of the transferrin receptor. Hence, restin may contribute to neoplastic transformation in Hodgkin's disease and anaplastic large cell lymphoma. Study of the mechanisms leading to restin overexpression may provide important data on the etiology of Hodgkin's disease and its relation to anaplastic large cell lymphoma.
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PMID:Restin in Hodgkin's disease and anaplastic large cell lymphoma. 816 33

A novel 160-kDa intermediate filament associated protein, named restin (Reed-Sternberg intermediate filament associated protein), is specifically expressed in the malignant cells of Hodgkin's disease and anaplastic large cell lymphoma (Ki-1 lymphoma). The combination of chromosomal R-banding and fluorescence in situ hybridization (FISH) with the use of two fluorescent dyes, fluorescein isothiocyanate and propidium iodide, allowed simultaneous detection of the hybridized DNA sequence and chromosomal R-banding. By this technique, the gene coding for restin (RSN) was assigned to chromosome region 12q24.31-->q24.33, while localization of the alpha-2-macroglobulin receptor (A2MR) was refined to 12q13.1-->q13.3. To further analyze the restin gene, a 500-kb YAC clone containing the gene was isolated and analyzed. A restriction map of this area is presented.
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PMID:Localization of the gene (RSN) coding for restin, a marker for Reed-Sternberg cells in Hodgkin's disease, to human chromosome band 12q24.3 and YAC cloning of the locus. 822 54

Fifty cases of extranodal non-Hodgkin's lymphoma arising in the oral cavity were reclassified using the updated Kiel classification. In order to determine the antigenic phenotype of the proliferating cells in oral lymphoma, we used a panel of paraffin effective antibodies that are known to react with lymphocyte- and histiocyte-associated antigens. The median age of the patients was 53 years, with a male predominance (M:F = 1.9: 1). The great majority of oral non-Hodgkin's lymphomas were B-cell lymphomas. There were 12 low-grade B-cell lymphomas (comprising one mucosa-associated lymphoid tissue, four centrocytic and seven centroblastic-centrocytic lymphomas) and 25 high-grade tumors (comprising 17 centroblastic, two immunoblastic, two Burkitt's and four lymphoblastic lymphomas). All 37 B-cell malignancies showed reactivity for L 26 and KiB 3. A monotypic immunoglobulin staining pattern, as revealed by light chain restriction, was found in 21 cases (57%) of the non-Hodgkin's lymphomas confirming their B-cell origin. Furthermore, monotypic staining for kappa-chain predominated (16/21 kappa, 5/21 lambda). Only a small number (6 cases) was of T-cell lineage and all cases showed positive reaction for UCHL 1, MT 1 and DFT 1. In one of six T-cell lymphomas, Ber-H 2 positive anaplastic large cell lymphoma was detected. Such a case was documented for the first time in the primary extranodal non-Hodgkin's lymphoma of the oral cavity. Five cases could be assigned with certainty to the histiocytic system. These cases were positive for cathepsin D and KP 1 LN 3, which recognized Ia (HLA-DR) antigens, was demonstrated most frequently in high-grade B-cell lymphomas, T-cell lymphomas and true histiocytic lymphomas.
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PMID:Immunophenotypic analysis of extranodal non-Hodgkin's lymphomas in the oral cavity. 833 73

Hodgkin (H) and Reed-Sternberg (RS) cells are considered to be the malignant cell population in Hodgkin's disease (HD). To date, their analysis has been hampered by their scarcity in primary tumors, poor growth in vitro, and lack of an animal model. To establish an in vivo system for the characterization of the malignant cells in HD, tumor biopsy samples from 13 HD patients were transplanted beneath the renal capsule or into the liver of severe combined immunodeficient (SCID) mice. HD-derived tissue from three patients gave rise to human tumors in SCID mice. Three different histologic patterns were observed: (1) lymphoproliferative disease (LPD), (2) anaplastic large cell lymphoma (ALCL), (3) Hodgkin-like lesions (HDLL). Immunohistochemical analysis showed that the tumors consisted of activated B cells (CD30+, CD20+). Epstein-Barr virus (EBV)-encoded transcripts were found in 80% to 100% of the tumor cells, although H and RS cells in the primary tumors of two patients were EBV-. All tumors examined (3 of 3) and the majority (6 of 10) of cell lines recultured in vitro had an abnormal karyotype. Southern blot analysis of the human Ig heavy chain gene showed that monoclonal or oligoclonal tumors of different B-cell origin grew in the SCID mice from the same germ line-configurated primary biopsy specimen. Our data suggest that the human cells in the SCID mice have either been derived from EBV superinfected H and RS cells or from EBV-infected bystander cells. If the latter is true, then these bystander cells must be genetically abnormal. The genetic defect would be either aneuploidy or instable euploidy. In either case, the cells might proliferate into malignant aneuploid HDLL or ALCL under the influence of EBV and the special environment encountered in the SCID mice.
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PMID:Hodgkin's lymphoma-derived tissue serially transplanted into severe combined immunodeficient mice. 835 87

Phenotypic, genotypic, and karyotypic analyses have indicated that Hodgkin's disease and CD30+ anaplastic large cell lymphoma may be conceived as malignancies derived from activated, cytokine-producing lymphoid cells, in many instances with an immature genotype. Most recently, Epstein-Barr virus (EBV) genomes and gene products, most notably the transformation-associated latent membrane protein (LMP), have been detected in approximately 50 and 20% of the cases, respectively. These findings suggest that EBV may superimpose an activated phenotype on an immature lymphoid cell, contributing to the pathoetiology of sizable proportions of these CD30+ malignancies.
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PMID:Epstein-Barr virus and CD30+ malignant lymphomas. 838 May 46

In 1985, Stein et al. (Blood 66:848-858) described a large cell lymphoma consisting of activated lymphoid elements, expressing the Reed-Sternberg cell-associated antigen Ki-1 (CD30); this tumor has recently been included in the updated Kiel classification and has been termed anaplastic large cell lymphoma (ALCL). This report concerns 13 patients with previously untreated ALCL who were admitted to the Pediatric Hematology and Oncology Department of Bologna University between January 1983 and December 1989. Ten cases were diagnosed as common type ALCL, 1 as Hodgkin's-related ALCL and the remaining 2 as histiocyte-rich ALCL/lymphohistiocytic T-cell lymphoma. T-cell markers were present in 85% of the cases, and B phenotype in the remaining 15%. About one-half of the patients presented systemic symptoms; all but one showed more than one involved site, mostly an association of nodal and extranodal sites. All patients (1 in stage I, 7 in stage II, and 5 in stage III) were treated with a modified version of the LSA2-L2 protocol. Survival and event-free survival at 4 years were 100% and 62.9%, respectively. Two out of 3 relapsed patients presented a recurrence of disease when they were off-therapy 24 and 36 months after first complete remission. Good response to salvage chemotherapy of all the relapsed patients and the long duration of the second complete remission were a distinctive characteristic of this neoplasm when compared to other histological subtypes. The clinical presentation, the tendency to develop late relapses and to achieve and maintain second remission easily suggest that ALCL is a high grade non-Hodgkin's lymphoma, from the histological point of view, but is similar to Hodgkin's disease from the clinical point of view. This would confirm the hypothesis that Hodgkin's disease and ALCL represent a continuous spectrum of the same disease.
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PMID:Anaplastic large cell lymphoma (Ki-1+/CD30+) in childhood. 839 Jun

CD30+ anaplastic large cell lymphoma (ALCL) represents a novel lymphoma entity at the borderline between Hodgkin's disease and non-Hodgkin's lymphomas. Phenotypic, genotypic, and karyotypic analyses have shown that ALCL are heterogeneous in cellular origin, and may be conceived as malignancies derived from activated, mainly T- or B-lymphoid cells, in some instances with an immature genotype. Epstein-Barr virus genomes and gene products, most notably the transformation-associated latent membrane protein (LMP), have been detected in a proportion of cases, and some cutaneous ALCL proved to harbor complete or incomplete HTLV-1 proviruses. These findings suggest that both EBV and HTLV-I, which are powerful inducers of CD30 expression in lymphoid cells in vitro, may contribute to the pathoetiology of ALCL.
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PMID:Tumor viruses in CD30-positive anaplastic large cell lymphomas. 839 68

Cytokines play important roles in the pathogenesis of lymphomas. Cytokines either can be produced or exert effects on neoplastic or reactive cells. The secretion of cytokines can provide growth advantages for tumor cells in either an autocrine or a paracrine fashion. An elevated serum or tissue level of cytokines can contribute to the clinical and histopathologic alterations associated with malignant lymphomas. The effects of cytokines on the histopathologic changes are most noticeable in Hodgkin's disease (HD). The malignant (Hodgkin's-Reed-Sternberg) cells in HD have been shown to secrete interleukin-1 (IL-1), IL-5, IL-6, IL-9, tumor necrosis factor-alpha, macrophage colony-stimulating factor, transforming growth factor-beta, and, less frequently, IL-4 and granulocyte colony-stimulating factor. These cytokines may be responsible for the increased cellular reaction and fibrosis observed in tissues involved by HD and for the immunosuppression in patients with HD. In contrast to Hodgkin's-Reed-Sternberg cells, most non-HD lymphoma cells do not produce cytokines in excess amounts. Exceptions include T-cell-rich B-cell lymphoma (IL-4), angioimmunoblastic lymphadenopathy-like T-cell lymphoma with plasmacytosis and hypergammaglobulinemia (IL-6), anaplastic large-cell lymphoma (IL-9), polymorphic immunocytoma (IL-6), and immunoblastic lymphoma (IBL) (IL-6). Some cytokines are involved in the unique cellular reactions in each of these types of lymphoma. For example, IL-4 is responsible for the T-cell reaction in T-cell-rich B-cell lymphoma, while IL-6 is accountable for the plasma cell reaction in angioimmunoblastic lymphadenopathy-type T-cell lymphoma. Others may be directly involved in the tumor cell growth or differentiation. For instance, IL-9 may be important for the autocrine proliferation of anaplastic large cell lymphoma, whereas IL-6 is essential for plasmacytoid differentiation in polymorphic immunocytoma. Further studies of the roles of cytokines in lymphomas may lead to major advances in the understanding of the molecular processes involved in the histopathogenesis of malignant lymphomas. Elucidation of the autocrine or paracrine function of cytokines also may lead to new approaches to a rational intervention in these disease processes.
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PMID:Cytokines in malignant lymphomas: review and prospective evaluation. 840 14


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