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)

Glycosaminoglycan and core protein components of proteoglycans (PGs) have been studied in three human non-Hodgkin lymphoma xenografts of B cell origin. Lymphomas showed similar GAG content, but different composition of GAG subtypes. This variability was accompanied by an individual capacity to adhere to extracellular matrix elements. The core proteins identified by monoclonal antibodies raised against human cartilage chondroitin sulfate PG were also distinctly expressed and released. These proteins shared by different cell types may have biological significance.
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PMID:Epitopes of cartilage core proteins and GAG pattern in human non-Hodgkin lymphoma xenografts. 171 29

A family of mono- and polyclonal antibodies raised against proteoglycans or their "subcomponents" served as novel markers to characterize the phenotypes of three non-Hodgkin lymphoma xenograft lines (HT 58 lymphoblastic, HT 117 centroblastic, HT 130 centrocytic) together with normal, human peripheral blood B lymphocytes. These xenografted NHL lines, maintained by serial transplantations on artificially immunosuppressed mice, expressed very similar B-cell-related antigens and differences on the cell surface (HT 58 greater than HT 117 greater than HT 130 greater than B cells) when they were exposed to monoclonal antibodies (mAb) to cartilage proteoglycans. Anti-proteoglycan antibodies used in this study recognize complex epitopes of core protein segment associated with carbohydrate, shared by human cartilage proteoglycans and certain lymphoma cells. The binding of these antibodies was independent of cell-cycle phase. The results suggest that the anti-proteoglycan mAbs could be used as new phenotypic markers to individualize non-Hodgkin lymphomas.
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PMID:Proteoglycan-targeted antibodies as markers on non-Hodgkin lymphoma xenografts. 228 6

Because of the T-cell abnormalities observed in Hodgkin's disease and the growing number of Hodgkin's disease cases observed in association with the acquired immunodeficiency syndrome (AIDS), concern has been expressed that a retrovirus may be the primary cause of Hodgkin's disease. We examined plasma specimens from 17 patients with Hodgkin's disease that were drawn in 1979. Because serum containing antibodies to either human T-lymphotropic virus type I (HTLV-I) or HTLV-II precipitate the major core protein, p24, of HTLV-I, lack of reactivity to HTLV-I p24 in all the specimens demonstrated absence of antibodies to HTLV-I or -II. None of the specimens was reactive to human immunodeficiency virus type 1 (HIV-1) by ELISA. None of the specimens were reactive on Western blot assays for HTLV-I or -II or HIV-1. Lack of evidence of cross-reacting antibodies to prototype strains of those retroviruses in specimens drawn before the AIDS epidemic suggests that classic Hodgkin's disease is not the result of infection with one of the known human lymphocytotropic retroviruses or a closely related agent.
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PMID:Lack of evidence of circulating retroviral antibodies in patients with classic Hodgkin's disease. 289 80

The HeFi-1 mAb recognizes a membrane protein on Hodgkin's disease cells and on a limited number of other human cells that are either tumorigenically transformed or virally activated. Herein biochemical and structural analyses of the HeFi-1 reactive membrane protein (HRMP) were done to identify its potential importance in cellular transformation in the Hodgkin's disease cell line L428, in the T cell lymphoma line HuT 78, and in several EBV-transformed lymphoblastoid cell lines. Immunoprecipitation studies demonstrated that the mature form of the HRMP had an apparent Mr of 120 kDa in tumor cells and 116 kDa in the EBV-transformed cell lines and that it was phosphorylated at both serine and tyrosine residues in all cell lines tested. The precursor to the HRMP is an 86-kDa core protein that, after processing by high mannose N-linked glycosylation, migrates with an apparent Mr of 90 kDa. This protein is then further processed to the mature 120-kDa HRMP in part by O-linked glycosylation, the addition of sialic acid residues, and by the conversion of N-linked oligosaccharides from the high mannose to the complex type. Detectable amounts of the 90-kDa molecule can be found in the membrane and, although this protein can be phosphorylated in vitro, it is not phosphorylated in intact cells. The combined results of this study suggest that the HRMP is involved in cellular metabolism and show that an unusual amount of post-translational processing of the 90-kDa precursor results in the formation, and perhaps phosphorylation, of the mature 120-kDa HRMP.
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PMID:Biochemical and structural properties of a Hodgkin's disease-related membrane protein. 338 12

Serologic testing shows that hepatitis C virus (HCV) may have a role in the pathogenesis of B-cell non-Hodgkin lymphomas (B-cell NHLs). We tried to demonstrate HCV RNA sequences in paraffin-embedded tissue from B-cell NHLs by reverse-transcription double polymerase chain reaction (RT-PCR) and Southern blotting. We studied 31 consecutive cases of B-cell NHLs; lymph nodes from 32 patients with diseases other than B-cell NHL were negative controls. Positive-strand HCV RNA was tested with primers for the 5' untranslated region. Replicative negative strand HCV RNA was tested with strand-specific RT-PCR for the 5' untranslated region. Immunohistochemical staining for HCV was done using an antibody to HCV core protein. Positive-strand HCV RNA was detected in 8 patients with B-cell NHL; negative-strand HCV RNA was detected in 6 of these cases, indicating viral replication. All control cases were negative for HCV RNA. Immunohistochemistry showed no staining of lymphoma cells for HCV core proteins in any case. HCV and B-cell NHLs may be associated. RT-PCR on paraffin-embedded lymphoma tissue is an alternative method of testing for HCV. The value of immunohistochemistry could not be ascertained. The exact role of HCV in the pathogenesis of B-cell NHL needs to be studied further.
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PMID:Detection of hepatitis C virus RNA sequences in B-cell non-Hodgkin lymphoma. 1070 20

Syndecans, transmembrane proteoglycans, play an important role in cell-matrix and cell-cell interactions, as well as modulators in receptor activation. These functions are partly non-specific and related to the heparan sulfate chains attached to the ectodomain, and partly specific due to the transmembrane and cytoplasmic domains of the core protein. In hemopoietic cells syndecan-1 is expressed only in B cells at certain differentiation stages (pre-B and plasma cells). In lymphoproliferative conditions this selective expression is retained in myelomas/plasmacytomas and other lymphoplasmacytic NHL subtypes, and primary effusional lymphomas. It is probably gained in B-CLL, and lost in other NHLs of pre- or post-follicular origin. It is concluded from these empiric results that the expression of syndecan is essential for some NHLs, probably ensuring the required connections to the microenvironment. From a diagnostic point of view, syndecan-1 is a very useful phenotypic marker to indentify cells with plasmacytic differentiation. The importance of syndecan expression in CLL and Hodgkin's lymphoma still requires further studies.
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PMID:Syndecans and the lymphoid system. 1083 Jul 34

Syndecans, transmembrane heparan sulfate proteoglycans, play an important role in cell-cell and cell-matrix interactions, as receptors/co-receptors of matrix elements, cytokines, growth factors. These functions are partly non-specific and due to the heparan sulfate chains attached to the ectodomain, and partly specific related to the transmembrane and cytoplasmic domains of the core protein. In hemopoietic cells syndecan-1 is expressed in certain B cells, in pre-B cells and plasma cells. In lymphoproliferative diseases this normal syndecan-1 expression of plasma cells is retained in myelomas/plasmocytomas, other lymphoplasmocytic NHL subtypes and primary effusional lymphomas. Syndecan-1 expression is probably gained in B-CLL, and lost in other NHLs of pre- or post-follicular origin. These results suggest that the expression of syndecan is essential for some NHLs, probably ensuring the required connections to the microenvironment. From a diagnostic point of view, syndecan-1 is a very useful phenotypic marker to identify cells with plasmocytic differentiation. The importance of syndecan expression in CLL and Hodgkin-lymphoma still requires further studies.
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PMID:[The role of syndecans in lymphoid systems] 1205 Jul 31

The aim of this study is to detect the possible role of hepatitis C Virus (HCV) in lymphomagenesis. HCV-RNA and anti-HCV antibodies were studied in tissue and serum samples taken from patients with non-Hodgkin's Lymphoma (NHL). The prevalence of HCV, the clinical presentation of these cases, and association with histologic subtypes were determined. RT-PCR was used to detect the HCV-RNA in serum and tissue samples. The anti-HCV antibodies were tested with microparticle enzyme immunoassay. Immunohistochemistry with the ABC method was used to detect the HCV core protein in HCV-RNA(+) cases. RNA could be detected in 30 of 35 cases, and other tests were performed in these 30 samples. HCV-RNA was detected in 11 tissue samples (11/30, 37%). HCV core protein was studied in 10 of 11 HCV-RNA(+) cases, and 1-3% nuclear staining was found in only 2 samples. Serologically, HCV-RNA was detected in 7 of 30 samples (23.3%) and anti-HCV antibody was detected in 3 of 30 samples (10%). Detection of HCV-RNA in 37% of the lymphoma tissue samples suggests that HCV may have a role or is a contributing factor in the pathogenesis of lymphoma. The very low HCV core protein in lymphoma tissues may be due to the low viral load in lymphoid tissues and/or higher sensitivity of the PCR method. Detection of anti-HCV antibody in only three cases may be associated with undetectable levels of antibodies due to the immune deficiency in cases with NHL.
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PMID:Detection of hepatitis C virus RNA in paraffin-embedded tissues from patients with non-Hodgkin's lymphoma. 1522 61

HCV chronic infection leads to liver diseases and also to a wide range of extrahepatic disorders including benign, but pre-lymphomatous forms (mixed cryoglobulinemia) to frank hematological neoplasia (non-Hodgkin's lymphoma). Recent data showed the involvement of p53 superfamily members in the pathogenesis of different lymphatic malignancies. In fact, tymomas and a subset of non-Hodgkin's lymphomas (NHLs) express high levels of p63. Thus, we analyzed whether alterations in p53 superfamily gene expression are observable in B lymphocytes isolated from HCV-infected patients with and without lymphoproliferative disorders. We showed, by real-time PCR, a significant induction of DNp63 mRNAs in B lymphocytes obtained from HCV-positive low grade non-Hodgkin's lymphoma patients. Since our current understanding of HCV proteins emphasizes the ability of the HCV core protein to deregulate the expression and activity of p53-related proteins, we established different B lymphocyte cell lines (Wil2-ns, Daudi and Ramos) stably expressing HCV core protein, in order to investigate the possible involvement of the viral protein in the upregulation of DNp63 in B lymphocytes. The analysis of p63 family transcripts showed no transcriptional changes for the p63 TA isoforms, whereas an increase (>5 times) of DNp63 mRNA occurred. In all cell lines, this abnormal expression was associated with a significant increase of cell proliferation that was specifically inhibited by silencing DNp63 mRNA. These findings suggest a pathogenetic role of the HCV core in HCV-related lymphomagenesis, through the induction of DNp63's pro-proliferative effects.
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PMID:Hepatitis C virus core protein enhances B lymphocyte proliferation. 1793 28

Hepatitis C virus (HCV) infection is associated with the development of hepatocellular carcinoma and probably also non-Hodgkin's B-cell lymphoma. The molecular mechanisms of HCV-associated carcinogenesis are unknown. Here we demonstrated that peripheral blood mononuclear cells obtained from hepatitis C patients and hepatocytes infected with HCV in vitro showed frequent chromosomal polyploidy. HCV infection or the expression of viral core protein alone in hepatocyte culture or transgenic mice inhibited mitotic spindle checkpoint function because of reduced Rb transcription and enhanced E2F-1 and Mad2 expression. The silencing of E2F-1 by RNA interference technology restored the function of mitotic checkpoint in core-expressing cells. Taken together, these data suggest that HCV infection may inhibit the mitotic checkpoint to induce polyploidy, which likely contributes to neoplastic transformation.
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PMID:Hepatitis C virus causes uncoupling of mitotic checkpoint and chromosomal polyploidy through the Rb pathway. 1979 24


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