Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventy-four out of 113 sera from patients with infectious hepatitis, chickenpox, measles and mumps reacted with both smooth muscle and cytoplasmic filaments in cultured fibroblasts and neuroblastoma. Five out of eighty-five control sera also reacted in this way. That the cytoplasmic structures are intermediate filaments was suggested by their rearrangement into coils of perinuclear filaments in colchicine- or vinblastine-treated fibroblasts, but not in cytochalasin B-treated cells. The idenity of these structures was confirmed by the demonstration that the same structures reacted with the post-viral sera and a rabbit and human anti-intermediate filament antibody. Immunoabsorption studies showed that twenty-seven out of thirty-two positive sera were neutralised by skeletin, the intermediate filament protein from smooth muscle. In all but one of the sera, the antibody was IgM. Antibody titres fell in the second specimen in eleven out of fourteen pairs of acute and convalescent sera. The association between viral infections and autoantibodies suggest that production of antibodies suggests that production of antibody to intermediate filaments may be initiated by viruses.
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PMID:Viral infections and IgM autoantibodies to cytoplasmic intermediate filaments. 38 89

A girl developed subacute sclerosing panencephalitis (SSPE). Eight years earlier she had had measles infection contracted shortly after cytotoxic treatment and radiotherapy for a spinal neuroblastoma. The case illustrates that typical SSPE, like immunosuppressive measles encephalopathy, can arise after drug-induced immunosuppression, and supports the view that these diseases probably represent opposite ends of a spectrum induced by measles virus infection in an individual with some form of immunological deficiency.
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PMID:Subacute sclerosing panencephalitis after drug-induced immunosuppression. 50 19

Growth of two measles virus strains, the TYCSA and CAM, was compared in three continuous cell lines derived from the nervous tissues, human neuroblastoma IMR-32, human glioma 118MGC, and rat glioma C-6. The two human neural cells were shown to support the growth of both measles virus strains as efficiently as in the non-neural Vero cells. Different types of cytopathic effect (CPE) between the two virus strains were noticed in IMR-32 cells; the CAM strain induced strand-forming type CPE and the TYCSA strain giant-cell type CPE. As a difference of growth pattern between IMR-32 and 118MGC cells, virus antigen was demonstrated in both the nucleus and cytoplasm of 118MGC cells whereas virus antigen was present only in the cytoplasm of IMR-32 cells. In contrast to the productive infection in human neural cells, growth of both virus strains was restricted in rat glioma C-6 cells without showing CPE although the prolonged presence of virus antigens was demonstrated by the immunofluorescent technique.
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PMID:Growth of measles virus in continuous cell lines derived from the nervous tissues of human and rat. 51 97

A case of measles infection without a rash, which was followed by a severe encephalopathy after two months, is described in a 2 1/2 year old boy. At the age of 8 months he had been irradiated for an inoperable intrathoracic neuroblastoma, and at the time of exposure to measles he was being treated with cyclophosphamide and vincristine. This case closely resembles other cases recently described and termed immunosuppressive measles encephalopathy. The syndrome is believed to represent the effect of measles virus in patients with deficient cellular immunity induced by antineoplastic treatment. The importance of protecting children on immunosuppressive treatment for contracting measles is stressed.
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PMID:Immunosuppressive measles encephalopathy. 62 62

Five patients with an unusual encephalopathy, possible secondary to measles virus infection, are described. Features common to these patients are: an existing chronic disease, neurologic deterioration 2 1/2 to 6 months after a measles infection, and death several weeks later. These events occurred when the chronic disease (e.g. leukemia or neuroblastoma) was in remission. That the measles virus was the causative agent is suggested only by finding in brain and extracranial tissues intracytoplasmic and intranuclear inclusions which contained measleslike particles. Additional clinical features seen in each of the five patients were: seizures, hypertension, and the inappropriate secretion of antidiuretic hormone.
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PMID:Encephalopathy following measles infection in children with chronic illness. 127 Nov 91

The effect of persistent measles virus infection on the expression of major histocompatibility complex (MHC) class I antigens was studied. Mouse neuroblastoma cells C1300, clone NS20Y, were persistently infected with the Edmonston strain of measles virus. The persistently infected cell line, NS20Y/MS, expressed augmented levels of both H-2Kk and H-2Dd MHC class I glycoproteins. Activation of two interferon(IFN)-induced enzymes, known to be part of the IFN system: (2'-5')oligoadenylate synthetase and double-stranded-RNA-activated protein kinase, was detected. Measles-virus-infected cells elicited cytotoxic T lymphocytes that recognized and lysed virus-infected and uninfected neuroblastoma cells in an H-2-restricted fashion. Furthermore, immunization of mice with persistently infected cells conferred resistance to tumor growth after challenge with the highly malignant NS20Y cells. The rationale for using measles virus for immunotherapy is that most patients develop lifelong immunity after recovery or vaccination from this infection. Patients developing cancer are likely to have memory cells. A secondary response induced by measles-virus-infected cells may therefore induce an efficient immune response against non-infected tumour cells.
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PMID:Persistent measles virus infection enhances major histocompatibility complex class I expression and immunogenicity of murine neuroblastoma cells. 134 54

Application of neutralizing anti-hemagglutinin antibodies to mouse neuroblastoma cells (NS20Y/MS) persistently infected with measles virus (MV) leads to a significant reduction of viral structural proteins within 6 days. While the transcriptional gradient for MV-specific mRNAs remained unaffected upon antibody treatment, the total amount of MV-specific transcripts dropped by 80% after 24 h. The expression of genomic RNA was affected similarly, with slightly slower time kinetics. Both transcription and expression of the viral structural proteins could be completely reactivated when viral antibodies were removed from the tissue culture. The same findings could be obtained in rat glioma cells persistently infected with subacute sclerosing panencephalitis virus (C6/SSPE) but not in cells of nonneural origin. The data indicate that antibody-induced antigenic modulation affects the early stages of viral transcription within a few hours after the addition of antibodies and leads to an almost complete repression of viral gene expression in cells of neural origin.
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PMID:Antibody-dependent transcriptional regulation of measles virus in persistently infected neural cells. 150 Dec 88

The matrix (M) gene of a measles virus (MV) variant passaged in IMR-32 human neuroblastoma cells displays numerous uridine-to-cytosine transitions called biased hypermutation. Using an in vitro assay, we show that IMR-32 cells contain high levels of an activity which unwinds and irreversibly alters the base pairing of double-stranded RNA synthesized from the M gene of MV. This activity is found exclusively in the cellular nucleus and is present at a lower level in African green monkey kidney Vero cells. Experiments with mixed cell extracts suggest that the low activity in Vero cells is not due to inhibitory factors. These findings support the hypothesis that this RNA-modifying and -unwinding activity is responsible for biased hypermutation of MV strains that infect the central nervous system. Possible functions of this neural cell activity and implications for central nervous system disorders are discussed.
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PMID:Irreversible modification of measles virus RNA in vitro by nuclear RNA-unwinding activity in human neuroblastoma cells. 173 7

The effect of persistent measles virus infection on c-fos protooncogene and protein kinase C (PKC-I) gene expression in a murine neuroblastoma cell line was studied. Overexpression of c-fos protooncogene by infected NS20Y/MS cells was detected when compared with uninfected NS20Y cells. The level of PKC-I-specific mRNA was increased in infected NS20Y/MS cells. In addition, the level of total PKC activity in these cells was also enhanced. We conclude that persistent measles virus infection can alter both protooncogene expression and signal transduction in cells of neuronal origin.
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PMID:Effect of persistent measles virus infection on protein kinase C activity and c-fos protooncogene expression in neuroblastoma cells. 250 30

The matrix (M) genes of Yamagata-1 strain subacute sclerosing panencephalitis virus passaged in African green monkey kidney cells and human neuroblastoma cells displayed strikingly nonrandom sequence divergence. The genes of both substrains shared a large number of uridine (U) to cytidine (C) transitions, but the latter contained numerous additional U to C changes in a localized region. Over 90% of the additional mutations were identical to the hypermutated nucleotides in the M gene found in a measles inclusion body encephalitis case. The nonrandom nature, the apparent host dependency, and the abrupt boundaries of these mutations suggest that these mutations might be caused by an extrinsic biased mutational activity rather than intrinsic polymerase errors. This mutational activity might account for the extraordinarily high C to U ratios in the non-protein-coding regions of both the M and fusion genes of wild-type measles virus.
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PMID:Generalized and localized biased hypermutation affecting the matrix gene of a measles virus strain that causes subacute sclerosing panencephalitis. 258 12


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