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)

The authors report two cases of children suffering from Epilepsia Partialis Continua (EPC). The first case concerned a boy primarily affected by abdominal neuroblastoma and secondarily by bilateral EPC; "pallidal posture" was the prominent clinical feature. An acute measles encephalitis was diagnosed and the CT scan showed necrosis of the putamina. The second case concerned a girl suffering from increased intracranial pressure due to suprasellar craniopharyngioma. Seven days after intervention, Diabetes Insipidus and EPC appeared. Enlargement of rolandic and sylvian spaces and lacunar necrosis of the putamen on the left side were also evident on the CT scan. The authors emphasize the significance of occasional metabolic disturbances, especially natremia, in the development of EPC.
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PMID:Kojewnikow's Epilepsia Partialis Continua: two cases associated with striatal necrosis. 314 49

A mouse neuroblastoma cell line (clone NS20Y) is highly tumorigenic in syngeneic A/J mice. When this clone was persistently infected with measles virus (NS20Y/MS) it failed to grow or form tumors in conventional A/J or nude mice, even when large numbers of cells were inoculated. As doubling time, serum dependence, and anchorage-independent growth on agar did not differ significantly between NS20Y and NS20Y/MS, lack of tumorigenicity of the persistently infected cells is unlikely to be due to an intrinsic property of the cells. NS20Y/MS cells were found to be effectively rejected in athymic nude as well as conventional syngeneic mice. However, injection of mice with either anti-interferon or anti-asialo GM1 serum, both of which have been shown to deplete natural killer (NK) cells in vivo, enabled NS20Y/MS cells to form large tumors. Unexpectedly, treatment of mice with silica also allowed the NS20Y/MS cells to form tumors. Under these conditions, it was shown that silica caused a significant decrease in NK activity as late as 7 days after a single injection. Although NS20Y/MS were not susceptible to NK cell lysis in vitro, the in vivo data suggest that NK cells are in fact the prime mechanism in the rejection of this persistently virus-infected neuroblastoma cell line by athymic and conventional syngeneic mice. The results indicate that NK activity may be greater or more sensitively detected in vivo than in vitro.
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PMID:Persistent viral infection affects tumorigenicity of a neuroblastoma cell line. 387 58

Growth of cell-free subacute sclerosing panencephalitis (SSPE) virus was compared with that of measles virus in three human neural cell lines; neuroblastoma, oligodendroglioma, and glioblastoma. The Edmonston strain of measles virus replicated in these neural cells as efficiently as in Vero cells. In contrast, the growth of the Mantooth strain of SSPE virus was suppressed moderately in neuroblastoma cells and markedly in oligodendroglioma and glioblastoma cells in spite of the induction of apparent cytopathic effects in these cells. Virus adsorption, defective interfering particles, interferon, and temperature sensitivity were not responsible for this low yield of SSPE virus in neural cell lines. Synthesis of viral proteins of SSPE virus was slower than that of measles virus in oligodendroglioma and glioblastoma cells. These results suggest that the slow rate of synthesis of viral proteins may be relevant to the low yield of SSPE virus in neural cells.
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PMID:Growth of measles and subacute sclerosing panencephalitis viruses in human neural cell lines. 608 91

Clone NS20Y of the mouse neuroblastoma C1300 was infected with wild-type Edmonston measles virus, and, after a transition to a carrier culture, became persistently infected. Persistently infected clones were derived and characterized morphologically by the appearance of multinucleate giant cells and nucleocapsid matrices in cytoplasm and nucleus, but very few budding virus particles. Antimeasles antibodies markedly suppressed the expression of viral antigens and giant cells, and the effect was totally reversible. When the cells were cultured at 33 degrees C, the number of giant cells began to diminish and ultimately disappeared; in contrast, when cultured at 39 degrees C, the cultures invariably lysed. Yields at 33 degrees C were ca. 2 logs lower than those at 39 degrees C. Cells cultured at 33 degrees C produced relatively high levels of interferon, whereas those at 39 degrees C produced little or no interferon. When the persistently infected cultures were exposed to anti-interferon alpha/beta serum at a nonpermissive temperature, there was a marked increase in multinucleate cells, suggesting that maintenance of the persistence state and its regulation by temperature may be related to the production of interferon. Viral isolates from cells cultured at 39 degrees C were obtained, and 90% of viral clones were found to be cold sensitive. Complementation studies with different viral clones indicated that the cold-sensitive defect was probably associated with the same genetic function. Western blot analysis of the persistently infected cells indicated a significant diminution and expression of all measles-specific proteins at a nonpermissive temperature. Infection of NS20Y neuroblastoma cells with the cold-sensitive virus isolates resulted in the development of an immediate persistent infection, whereas infection of Vero or HeLa cells resulted in a characteristic lytic infection, suggesting that the cold-sensitive mutants may be selected or adapted for persistent infection in cells of neural origin.
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PMID:Isolation of cold-sensitive mutants of measles virus from persistently infected murine neuroblastoma cells. 620 37

The replication of measles virus in human neural and nonneural cell lines in terms of growth and cytopathic effect was affected by treatment of the cells with papaverine, which increases endogenous cyclic AMP. Suppression of virus growth was most prominent in neuroblastoma cells, followed by that in epidermoid carcinoma and glioblastoma cells, whereas the suppressive effect was relatively weak in oligodendroglioma cells. The papaverine-induced suppression of virus growth in neuroblastoma cells was studied in detail. The suppression that occurred was dependent on the dose of papaverine and was reversible. By treatment with 10 microM papaverine, virus-cell interactions were modified as follows: (i) early replication steps such as adsorption, penetration, and uncoating of the virus were not affected; (ii) synthesis of viral RNAs, including genomic RNA and mRNA, was inhibited; (iii) translation of viral proteins from mRNA was not blocked; and (iv) glycosylation and transport of viral glycoproteins to the cell membrane were not inhibited, but phosphorylation was blocked. The significance of suppressed virus replication in neural cells is discussed in relation to the persistence mechanisms of measles virus in the central nervous system.
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PMID:Effect of papaverine treatment on replication of measles virus in human neural and nonneural cells. 670 72

Subacute sclerosing panencephalitis is a slowly progressing fatal human disease of the central nervous system which is a delayed sequel of measles virus (MV) infection. A typical pathological feature of this disease is the presence of viral ribonucleocapsid structures in the form of inclusion bodies and the absence of infectious virus or budding viral particles. The mechanisms governing the establishment and maintenance of a persistent MV infection in brain cells are still largely unknown. To understand the mechanisms underlying MV persistence in neuronal cells, a tissue culture model was studied. Clone NS20Y/MS of the murine neuroblastoma C1300 persistently infected with the wild-type Edmonston strain of MV secretes relatively high levels of alpha/beta interferon (IFN). As shown previously, treatment of the persistently infected cultures with anti-IFN serum converted the persistent state into a productive infection indicated by the appearance of multinucleated giant cells. In this study, we have investigated whether alpha/beta IFN produced by NS20Y/MS cells activates cellular protein tyrosine kinases which will induce tyrosine phosphorylating activity specific to virus-infected cells. We present data to show augmented protein tyrosine kinase activity in the persistently infected cells. We demonstrate that the MV N protein is phosphorylated on tyrosine in addition to serine and threonine in the persistent state but not in NS20Y cells acutely infected with MV.
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PMID:Tyrosine phosphorylation of measles virus nucleocapsid protein in persistently infected neuroblastoma cells. 788 96

To investigate the effect of persistent measles virus infection on signal transduction in cells of neuronal origin, the mouse neuroblastoma cell line NS20Y/MS, which is persistently infected with measles virus, was used. The results demonstrate an approximate 50% increase in total phosphorylation and a similar increase in protein kinase C (PKC) activity. Western blot analysis with anti-total PKC or anti-PKC-alpha antibodies revealed a significant increase in the level of an 80K immunoreactive PKC in NS20Y/MS cells. Following incubation of NS20Y/MS cells with polyclonal anti-measles virus antibodies, which down-regulate the level of measles virus proteins, total and PKC-mediated phosphorylation returned to the basal level of uninfected cells. This effect was reversible and removal of the antibodies resulted in restoration of the high level of total and PKC-mediated phosphorylation. The release of infectious measles virus was strongly inhibited by incubation of NS20Y/MS cells with the PKC inhibitor, 1-(5-isoquinolinylsulphonyl)-2-methylpiperazine (H-7). These results demonstrate that measles virus induces elevation in cellular phosphorylation which is essential for measles virus production.
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PMID:Reversal of the measles virus-mediated increase of phosphorylating activity in persistently infected mouse neuroblastoma cells by anti-measles virus antibodies. 815 Dec 98

Replication and encapsidation of measles virus (MV) requires the interaction between the nuclear protein (N) and the phosphoprotein (P). It is known that both proteins are phosphorylated on serine and threonine residues. Recently we have shown that N is phosphorylated on tyrosine in persistently-infected mouse neuroblastoma cells (NS20Y/MS). Here, we show that P in NS20Y/MS is also phosphorylated on tyrosine. To investigate whether cellular tyrosine kinases can bind and phosphorylate P, a solid phase kinase assay was employed. We show that bacterially-expressed MV P fragments, were phosphorylated on tyrosine by purified mouse c-Src protein-tyrosine kinase and when mixed with uninfected neuroblastoma cell (NS20Y) extracts, these P fragments were phosphorylated on tyrosine in addition to serine and threonine. These results imply that MV P is a substrate for tyrosine phosphorylation by cellular tyrosine kinase(s).
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PMID:Tyrosine phosphorylation of measles virus P-phosphoprotein in persistently infected neuroblastoma cells. 903 64

Biased hypermutation events found predominantly in the matrix gene of measles virus isolated from persistent human CNS infections have been attributed to the action of a cellular unwinding/modifying activity (UMA). To define the level and distribution of this activity in brain cells, fractionated extracts were prepared from the nuclei and cytoplasm of human glioblastoma (D-54, U-251) and neuroblastoma (IMR-32, SKN-MC) cells and analyzed for their ability to modify synthetic dsRNAs specific for the measles virus (MV) matrix (M) gene. On a quantitative basis we could show that the activity localized to both the nuclear and cytoplasmic compartments of both cell types analyzed independent of cell proliferation. The presence of significant levels of UMA in the cytoplasm of human brain cells following growth arrestment in vitro with retinoic acid supports the interpretation that UMA may contribute to the attenuation of MV gene functions during the primary infection of brain cells, thereby supporting the establishment of virus persistence.
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PMID:Measles virus-specific dsRNAs are targets for unwinding/modifying activity in neural cells in vitro. 922 45

Measles virus (MV) persistence in brain cells has broad effects on different cellular functions. We have previously shown that NS20Y clone, originally derived from C1300 neuroblastoma cells, persistently infected with MV (NS20Y/MS), displays constitutively elevated levels of c-fos and PKC mRNAs, implying MV-mediated effects on transcriptional regulation. Nonetheless, the mode by which virus affects the transcriptional machinery still remains obscure. In order to define this phenomenon, we studied the binding properties of major transcription factors (AP-1 and NFkappaB) in NS20Y/MS cells. Using electrophoretic mobility shift approach (EMSA) with the appropriate oligonucleotide probes, we have found that the persistent MV infection does not affect NFkappaB binding, while the AP-1 binding was significantly decreased. Similar inhibition was not observed in NS20Y cells acutely infected with MV. Anti-measles antibody-mediated restriction of viral gene expression restored AP-1 binding, thus suggesting that measles virus proteins may affect the components of the host transcriptional machinery.
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PMID:The effects of measles virus persistent infection on AP-1 transcription factor binding in neuroblastoma cells. 923 27


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