Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of 3 muM cortisol on cell proliferation in rat glioma (strain C6) monolayer cultures was investigated. Cell density measurements showed that cortisol-treated C6 cells continued to proliferate at maximum log phase rates for 1 to 2 days. Then cell proliferation ceased as growth in control cultures continued into stationary phase. A 2-day period of growth inhibition followed during which cell densities were 30 to 50% lower relative to controls. Growth resumed subsequently, and final cell densities were similar to those of controls. The presence of epicortisol (the biologically inactive isomer of cortisol) in the culture medium did not alter the rate of log phase growth relative to controls. During the initial period of continued growth after exposure to cortisol, the pH of the medium decreased at the same rate in control and treated cultures. During the growth-inhibitory period, erythrosin B dye was excluded equally well (greater than 94%) by control and treated cells, and no morphological differences were detected by phase contrast microscopy. When the culture medium was replaced daily, the control cells at elevated densities continued to proliferate at a reduced rate. In cortisol-treated cultures, the period of growth inhibition commenced 3 days after the cells were exposed initially to cortisol. A 2-day period of growth inhibition followed during which the pH of the 1-day-old media from both control and treated cultures decreased from 7.4 to 6.9. Growth resumed subsequently in the treated cultures to produce elevated cell densities similar to those of controls. These results demonstrate that cortisol at concentrations considered chemotherapeutic in vivo exerts a transient inhibitory effect on C6 glioma cell proliferation.
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PMID:Transient inhibition of cell proliferation in rat glioma monolayer cultures by cortisol. 0 44

The C6 glioma cell line contains nerve growth factor (NGF) which can be released into the medium. Treatment of the cells with beta-adrenoceptor agonists resulted in increased content of NGF in both the cells and the medium within a few hours, whereas alpha-adrenoceptor agonists were ineffective. The response was blocked by beta- but not alpha-adrenoceptor antagonists. The increase of the NGF content of glioma cells appeared to be mediated by an elevation of cyclic AMP or GMP. The addition to the cell cultures of other putative neurotransmitters failed to change the content of either NGF or cyclic AMP. These results are discussed with respect to a model for adrenergic neuron-glial interactions.
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PMID:Regulation of nerve growth factor content in C6 glioma cells by beta-adrenergic receptor stimulation. 2 24

Metabolic rates and intercellular transfer of metabolites were studied in human glia and glioma culture cells via topographic scan of NAD(P)H fluorescence by multichannel microfluorometry in conjunction with microinjection of glucose-6-P + allosteric activators. Metabolic rates evaluated from NAD(P) in equilibrium NAD(P)H transients and the required substrate levels were 3--4 times lower in glioma cells as compared to glia cells. Both glia and glioma cells showed variability in the occurrence of intercellular metabolite transfer, detectable via observation of a transient in a neighbour of the cell injected with substrate. On this basis "multicellular integrated states" can be defined in clusters of glioma and glia cells interconnected by cell-to-cell contact and a mesh-like network of intercellular processes. Such multicellular steady states and the associated metabolic rates or their impairment can be used in turn to classify different culture lines in reference to cell physiology and pathology.
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PMID:Metabolic rates and intercellular transfer of molecules in cultures of human glia and glioma cells. 3 40

Two novel beta-adrenergic myocardial stimulants of general structure: Formula: (see text), where R is a phenyl or benzyl group were investigated for their ability to stimulate and desensitize the cyclic AMP response of C6 glioma cells. Compound ICI 89, 963 (R:phenyl) which elicited less than 1% of the maximum increase in cAMP produced by isoproterenol, was strikingly effective as a desensitizer of the isoproterenol response. This desensitization was markedly reduced by propranolol. Compound ICI 119,033 (R: benzyl) which was a more effective stimulant of cAMP synthesis than ICI 89,963, was also a more effective desensitizer of the isoproterenol response of C6 cells. The kinetics of the desensitization by ICI 89,963 were comparable with those for isoproterenol reaching a maximum in 2 to 3 hours. The data indicate that beta-adrenergic agonists are more potent as desensitizers of the cyclic AMP response than as stimulants of that response.
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PMID:Desensitization of beta receptor mediated cyclic AMP response of cultured fibroblasts by partial agonists. 3 55

Different cholinergic cell lines were fused with an adrenergic neuroblastoma cell line (N115-BU-8). Its fusion with a cholinergic neuroblastoma-glioma hybrid produced a "hybrid-hybrid" line containing cholinergic and adrenergic enzyme activities. Both activities were also present in subclones of this line. The presence of catecholamines in single cells was confirmed by microspectrofluorimetry. These results are discussed with respect to the possibility of a simultaneous synthesis of noradrenaline and acetylcholine in single cells. The cholinergic and adrenergic enzyme activities are influenced by cell density, by dexamethasone, and by conditioned medium.
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PMID:Clonal hybrid cell lines expressing cholinergic and adrenergic properties. 4 Dec 46

The aminobenzyl analog of propranolol, 1- (p-amino-alpha,alpha-dimethylphenethylamino)-3-(1-naphthoxy)-2- propanol, was synthesized and found to be a potent beta-adrenergic blocking agent. The beta-adrenergic receptors of cultured rat C6 glioma cells (2B clone) as assessed by [(125)I]iodohydroxybenzylpindolol binding were decreased 50 and >95% after pretreatment with 8 nM and 1 muM aminobenzylpropranolol, respectively. Unlike propranolol, aminobenzylpropranolol displayed a prolonged blockade of receptors that was maintained during several hours of washing. [(125)I]Iodohydroxybenzylpindolol saturation binding experiments in cells exposed to aminobenzylpropranolol and subsequently washed indicated that the compound effectively diminished receptor number with no change in the affinity of the remaining receptors for iodohydroxybenzylpindolol. Aminobenzylpropranolol inhibited catecholamine-stimulated intracellular cyclic AMP accumulation; with increasing blockade, isoproterenol dose-response curves became progressively shifted to the right but the maximal response was unaltered. Aminobenzylpropranolol inhibited the beta-adrenergic contractile response in atria isolated from rats and guinea pigs. Treatment with 0.1 and 10 muM aminobenzylpropranolol produced decreases of 0.5 and 2 orders of magnitude in the contractile potency of isoproterenol. As in glioma cells, aminobenzylpropranolol failed to decrease the maximal response to isoproterenol. The effects of aminobenzylpropranolol persisted during extensive washing of atria (up to 17 hr). Repeated exposures to isoproterenol at concentrations sufficient to produce maximal tension development also failed to alleviate the blockade. The inotropic potency of histamine in guinea pig atria was not affected by aminobenzylpropranolol. These data suggest that catecholamines are capable of eliciting full biological responses in glioma cells and isolated atria even though the great majority of beta-adrenergic receptors are persistently blocked.
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PMID:Quantitative relationship between beta-adrenergic receptor number and physiologic responses as studied with a long-lasting beta-adrenergic antagonist. 4 15

Spleen cells from BDIX-rats bearing either GVlAl-tumor (a syngeneic mixed glioma) or NVlAc-tumor (a cloned syngeneic neurinoma of the peripheral nervous system) were cytotoxic to both tumor cells in vitro. However, the tumors displayed individually distinct antigenic specificities by in vivo rejection tests. Their in vitro cross-reactivity disappeared when a particular subpopulation of the spleen cells was used. The procedure of lymphocyte purification included three consecutive steps: treatment with carbonyl iron and magnetism, passage through a nylon wool column, and finally removal of complement receptor-bearing cells present in the colum-excluded population. Cross-reactivity between the syngeneic tumors persisted after the first two steps of lymphocyte purification. In contrast, specific cytotoxic reactions were observed against each individual tumor subsequent to the removal of the remaining C3 receptor-positive but surface Ig-negative cells. While killer cells were present in normal spleen-cell populations, these were almost completely eliminated by passage through the nylon wool column.
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PMID:Spleen-cell reactivity against transplanted neurogenic rat tumors induced by ethylnitrosourea: uncovering of tumor specificity after removal of complement-receptor-bearing lymphocytes. 5 Feb 96

2,2'-Anhydro-1-beta-D-arabinofuranosyl-5-fluorocytosine (anhydro-ara-FC) was compared with cytosine arabinoside (ara-C) in the treatment of ic implanted murine Glioma 261. Both drugs given in ip doses of 500 mg/kg immediately inhibited the uptake and incorporation of tritiated thymidine into the DNA of brain tumor, small intestine, and spleen. Inhibition of DNA synthesis in the tumor recovered within 12 hours of anhydro-ara-FC administration, yet it remained depressed greater than 50% of control 12 hours after ara-C administration. Inhibition in the small intestine recovered within 24 hours of drug administration with either agent while inhibition in the spleen remained depressed greater than 24 hours. Anhydro-ara-FC administered ip in single doses less than or equal to 1500 mg/kg or in multiple doses less than or equal to 200 mg/kg three times a week for ten doses failed to prolong the survival of tumor-bearing mice, and minimal increased survival followed drug administration of 200 mg/kg every 24 hours for five doses. In contrast, ara-C in doses of 50, 100, or 200 mg/kg three times weekly for ten doses significantly increased the survival of tumor-bearing animals between 17% and 36%.
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PMID:Comparison of 2,2'-anhydro-1-beta-D-arabinofuranosyl-5-fluorocytosine and cytosine arabinoside in the treatment of murine brain tumor. 6 95

Partial biochemical characterization of several neural tissue specific antigens isolated from a murine glioblastoma cell line was accomplished by means of radioiodination of intact cells followed by immunoprecipitation of the cell lysate with a rabbit serum specific for neural tissue antigens. Polyacrylamide gel electrophoresis of the immunoprecipitate in sodium dodecyl sulfate resolved the labeled antigens into several major components: two proteins (or glycoproteins) having apparent m.w.'s of 84,000 and 120,000 and lipid associated components which may be heterogeneous. The protein and lipid associated components apparently possess independent antigenicity because after chloroformmethanol extraction the protein components can be immunoprecipitated from the aqueous phase and the lipid associated component can be immunoprecipitated from the organic phase. Despite their independent antigenicity it is not known whether the components may be noncovalently associated on the cell surface. Although some of these antigens can be isolated from brain or glioma cells (a related tumor), non can be demonstrated in lymphoid tissues or C1300 neuroblastoma cells using identical methods. Therefore, these studies confirm our previous findings concerning the specificity of the anti-NS-2 antiserum by using cytotoxicity tests.
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PMID:Partial characterization of nervous system-specific cell surface antigen(s) NS-2. 6 27

A patient with a six-year history of seizures and a shorter history of a progressive hemiparesis, had a glioma. A partial frontal lobectomy was performed. The cerebrospinal fluid, 38 days post-operatively, prior to irradiation, had an increase in gamma globulins. Following cranial irradiation the CSF gamma globulin level returned to normal and the hemiparesis disappeared. The significance of these CSF changes is discussed.
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PMID:Elevated CSF gamma globulins with cerebral "glioma.". 7 79


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