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)

Polypeptides, characterized by their ability to confer a transformed phenotype on an untransformed indicator cell have been isolated directly from surgical specimens of intracranial meningioma by using an acid/ethanol extraction procedure. Transforming activity in meningeal cells was based on the ability to induce NRK 49F rat kidney fibroblasts to form colonies in soft agar. This polypeptide was separated by gel filtration into two fragments of 15 and 40 kilodalton (kDa) molecular weight. Among other cases of brain neoplasms, one case of glioblastoma multiforme had moderate TGF-beta activity, but medulloblastoma and neurinoma had no activity. Purified TGF-beta also stimulated DNA synthesis in primary cultured meningioma cells, but no effect was seen in U 251MG human glioma cells. While the physiological function of TGF-beta is still ill-defined and the molecular character of its receptor has not been analyzed, intracranial meningiomas are noted to have TGF-beta-like activity. TGF-beta also induces the DNA synthesis of cultured meningioma cells. From these results, TGF-beta would be considered one of the growth promoting factors in meningioma.
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PMID:Transforming growth factor (TGF)-beta like activity of intracranial meningioma and its effect on cell growth. 202 25

Ethanol has been shown to suppress calcium uptake into depolarized synaptosomes, to reduce the durations of calcium spikes in cultured cells and to reduce calcium conductances in invertebrate neurons. Voltage-activated calcium channels therefore appear to be an important target of ethanol action. However, the interactions of ethanol with specific types of calcium channels have yet to be defined. This study examined the effects of ethanol on two different populations of calcium channels in N1E-115 neuroblastoma and in NG108-15 neuroblastoma x glioma hybrid cells. Transient (type I) and long-lasting (type II) calcium channel currents were recorded with the whole-cell voltage clamp technique. At concentrations above 30 mM, ethanol reversibly suppressed both types of calcium channel currents, without changing the voltage dependence of activation. Concentration-response curves were essentially the same for type I and type II channels. Ethanol at concentrations of 100 and 300 mM blocked currents by approximately 15 and 40%, respectively. The voltage dependence of type I channel inactivation was not altered by ethanol concentrations as high as 300 mM, nor was there evidence of a use-dependent blocking action. The effects of ethanol on calcium channels were similar in NG108-15 cells; both channel types were blocked by ethanol at about the same concentrations as were effective in N1E-115 cells. Because ethanol interacts with opiate receptors in some systems, and leucine-enkephalin is known to block type II currents in NG108-15 cells, we examined whether the ethanol block of type II currents could be altered by naloxone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ethanol effects on two types of voltage-activated calcium channels. 216 82

Intermediate filament proteins are cytoskeletal components in most vertebrate eukaryotic cells and some of these proteins are recognized markers of cell differentiation. To investigate the expression of intermediate filament proteins of the S-phase cells in human glial tumors, we have examined fourteen patients with benign and malignant gliomas by immunohistochemical study using in vivo labeling with bromodeoxyuridine (BrdU). Five glioblastoma multiforme, five anaplastic astrocytoma, three fibrillary astrocytoma and one gemistocytic astrocytoma were studied. All patients were given intravenous infusion of BrdU (10 mg/kg) one hour before craniotomy for labeling the S-phase cells of the tumors. Surgical specimens were immersed in 70% ethanol, and embedded in paraffin. Four micron sections were immunostained with anti-BrdU monoclonal antibody (Mab) and anti-vimentin Mab by avidin-biotin complex (ABC) method, and anti-glial fibrillary acidic protein (GFAP) serum by peroxidase-antiperoxidase (PAP) method. All sections (except for case 4) were double-labeled with anti-BrdU Mab and anti-GFAP serum, or with anti-BrdU Mab and anti-vimentin Mab. The population of BrdU-labeled cells (i.e. S-phase cells), and double-labeled cells were analyzed. The proportions of BrdU-labeled cells ranged from 6.1% to 17.0% (average 11.1%) in glioblastoma multiforme, from 3.5% to 15.6% (average 8.8%) in anaplastic astrocytoma, and from 2.0% to 2.8% (average 2.5%) in fibrillary astrocytomas. One gemistocytic astrocytoma showed S-phase fraction of 1.7%. Two recurrent cases of anaplastic astrocytoma showed higher S-phase fractions than other non-recurrent cases of anaplastic astrocytoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunohistochemical study of S-phase cells in human gliomas]. 246 Jan 17

In this study, the effects of ethanol exposure on uptake and metabolism of arachidonic acid by C-6 glioma cells in culture was examined. Labeled arachidonic acid was effectively taken up by the phospholipids of these cells and radioactivity was initially incorporated into phosphatidylinositols and phosphatidylcholines, reaching a peak between 4 and 6 hours. However, the labeling of ethanolamine plasmalogens continued to show an increase with time after labeled arachidonic acid has been exhausted in the medium. Since over 90% of labeled arachidonic acid was already taken up by the cells after 4 hours of exposure, the continued increase in labeling of ethanolamine plasmalogens is attributed to a transacylation mechanism. Cells grown in 150 mM ethanol for 2 days did not show a change in the overall incorporation of labeled arachidonic acid into phospholipids but showed a significant increase in labeling of ethanolamine plasmalogens, which was marked by a concomitant decrease in labeling of phosphatidylcholines. Ethanol exposure also resulted in a significant increase in the transfer of labeled arachidonic acid to triacylglycerols. Changes in phospholipid and triacylglycerol labeling pattern positively correlated with increasing ethanol concentration from 75 to 300 mM. Besides, most ethanol effects were readily noticeable after 24 hours of exposure. These data suggest a specific effect of ethanol on promoting the transacylase process for biosynthesis of ethanolamine plasmalogens as well as the acyltransferase for biosynthesis of triacylglycerols.
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PMID:Ethanol alters the transfer of arachidonic acid to ethanolamine plasmalogens in C-6 glioma cells. 251 31

Cell proliferation potential was assessed by measuring the labeling indices of the monoclonal antibody Ki-67 and of 5-bromodeoxyuridine (BUdR), and the cellular deoxyribonucleic acid (DNA) content in 48 human brain tumors. The diagnostic and prognostic value of flow-cytometric DNA analysis was also evaluated using ethanol-fixed paraffin-embedded BUdR-labeled specimens; these were the same specimens as were used for measuring the BUdR and Ki-67 labeling indices. Both the Ki-67 and the BUdR labeling indices correlated with the degree of malignancy estimated from conventional histological preparations. The Ki-67 labeling index was 1.7 times greater than the BUdR labeling index. The relationship of DNA aneuploidy to the labeling indices or to morphology in cases of glioma was examined. All of the tumors with an aneuploid line corresponded to malignant glioma classified by histological criteria, although malignant glioma did not always show DNA aneuploidy. In addition, the cases with aneuploid lines showed high BUdR and Ki-67 labeling indices. The cell kinetic data, which indicate the biological character of tumors, allowed prediction of the prognosis of the patients with gliomas. In contrast, despite the presence of an aneuploid line, three of 13 meningiomas showed a benign histological pattern without an aggressive clinical course, and neither the Ki-67 nor the BUdR labeling index was high. These results indicate an unequivocal relationship between DNA aneuploidy and clinical behavior; in general, both labeling indices may prove to be objective indicators of the outcome of patients with brain tumors.
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PMID:Flow-cytometric DNA analysis and immunohistochemical measurement of Ki-67 and BUdR labeling indices in human brain tumors. 253 5

The effect of short-and long-term ethanol exposure on bradykinin-stimulated hydrolysis of phosphatidylinositol 4.5-bisphosphate (PIP2) was investigated in neuroblastoma X glioma hybrid cells (NG 108-15). Acute exposure of 50-150 mM ethanol neither influenced the bradykinin-stimulated accumulation of [3H]-inositol phosphates (IP1, IP2, IP3) nor the hydrolysis of PIP2 in cells labelled with [3H]-inositol. Furthermore, ethanol (100 mM) added in the absence of agonist did not influence these parameters. However, in cells cultivated for 4 days in 100 mM ethanol, PIP2 hydrolysis and IP1, IP2 and IP3 formation after stimulation by 10(-6)-10(-5) M bradykinin was markedly inhibited while there was no effect on the basal levels or on the levels found after stimulation with low concentrations of bradykinin. The inhibitory effect of ethanol on IP accumulation became significant after 2-3 days of ethanol.
Alcohol
PMID:Ethanol effects on bradykinin-stimulated phosphoinositide hydrolysis in NG 108-15 neuroblastoma-glioma cells. 255 51

Late passage C-6 glioma cells exhibit astrocytic properties as shown by a characteristic cell morphology and by high levels of the astrocytic cell maker glutamine synthetase (GS). In this study the effects of ethanol (0.2%-1.0% w/v) on the pattern of dibutyryl cyclic AMP (dBcAMP, 1 mM)-induced differentiation were examined using cell number and DNA content as indices for proliferation and cell morphology and GS activity to evaluate differentiation. Differences were observed in the susceptibility of cells to dBcAMP alone, ethanol alone, or simultaneous exposure to both drugs, when cultures were compared at logarithmic and postconfluent phases of growth. Exposure to dBcAMP decreased cell proliferation, induced a characteristic change in cell shape and increased GS activity. In logarithmic phase, simultaneous exposure of cells to ethanol and dBcAMP delayed the dBcAMP-induced change in cell shape and attenuated the mitosis-restricting properties of exposure to dBcAMP. Furthermore, GS activity was greater in dually treated cultures than in cultures treated with dBcAMP alone. We interpret this higher enzyme activity to be the consequence of increased cell-cell contact resulting from larger numbers of cells in the dually treated cultures, coupled with a subsequent dBcAMP-induction of this cytosolic enzyme. In postconfluent cultures, ethanol-exposure did not statistically alter DNA content; whereas GS activity was lower, suggesting that synthesis of GS may be impaired by cellular exposure to ethanol. Furthermore, enzyme activity was also lower in cultures treated with dBcAMP in concert with ethanol than in those treated with dBcAMP alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responses in astrocytic C6 glioma cells to ethanol and dibutyryl cyclic AMP. 286 87

Ethanol inhibits opioid peptide binding to the delta-opioid receptor. When neuroblastoma x glioma NG108-15 hybrid cells are grown with 25-200 mM ethanol, opioid receptor density increases up to 2-fold without a change in receptor affinity. Since changes in neurotransmitter receptor density may be important in neuronal adaptations to ethanol, we investigated the underlying mechanisms and functional consequences of this phenomenon. The opiate antagonist, naloxone, also increased opioid receptor number, but produced a smaller effect than ethanol with greater fractional inhibition of binding; long term enhancement of binding by ethanol is therefore not a simple function of acute receptor inhibition. Ethanol did not inhibit receptor down-regulation by etorphine, an opiate agonist, and therefore is not likely to increase receptor expression through interference with tonic down-regulation by endogenous opioid peptides. Ethanol increased opioid receptor expression in NG108-15 cells treated with actinomycin D, but not cycloheximide; hence, normal protein synthesis, but not DNA transcription, may be required for this response. The opioid receptors induced in ethanol-treated cells were subject to normal up-regulation by naloxone, down-regulation by etorphine, and acute inhibition of agonist binding by Na+. Etorphine maximally inhibits cyclic AMP accumulation in NG108-15 cells with only fractional occupancy of opioid receptors. Chronic ethanol exposure increased the receptor reserve for this response, resulting in a 3.5-fold increase in the potency of etorphine for inhibiting phenylisopropyladenosine-stimulated cyclic AMP accumulation. Neuronal adaptation to ethanol may involve changes in the density of receptors that regulate cellular levels of cyclic AMP.
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PMID:Ethanol increases the expression of functional delta-opioid receptors in neuroblastoma x glioma NG108-15 hybrid cells. 300 82

The acute and chronic neurologic effects of ethanol appear to be due to its interaction with neural cell membranes. Chronic exposure to ethanol induces changes in the membrane that lead to tolerance to the effects of ethanol. However, the actual membrane changes that account for tolerance to ethanol are not understood. We have developed a model cell culture system, using NG108-15 neuroblastoma-glioma hybrid cells, to study cellular tolerance to ethanol. We have found that adenosine receptor-stimulated cAMP levels increased markedly upon acute exposure to ethanol. However, the cells became tolerant to ethanol, since chronically treated cells required ethanol to maintain normal adenosine-stimulated cAMP levels. Moreover, the cells appeared to be dependent on ethanol, as evidenced by reduced adenosine-stimulated cAMP levels in the absence of ethanol. Recovery occurred after ethanol was withdrawn. These cellular changes appear to parallel the clinical events of acute ethanol intoxication, tolerance, and dependence.
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PMID:Ethanol regulation of adenosine receptor-stimulated cAMP levels in a clonal neural cell line: an in vitro model of cellular tolerance to ethanol. 300 52

Long-term incubation of clonal neural cell lines with ethanol differentially reduces the stimulation of cAMP accumulation by hormones and cholera toxin. In the NG108-15 neuroblastoma chi glioma hybrid cell line, this heterologous desensitization was associated with a 42% reduction in the expression of Gs alpha and no significant change in Gi alpha. By contrast, ethanol treatment of the parental neuroblastoma cell line N18TG2 caused little loss of response to hormones or cholera toxin and no significant change in Gs alpha or Gi alpha. Ethanol induced heterologous desensitization in N1E-115 neuroblastoma cells; however, this cell line showed a dose-dependent increase in Gi alpha and a later decrease in Gs alpha. Thus, ethanol causes heterologous desensitization of hormone-stimulated cAMP accumulation by different mechanisms in related neural cell lines.
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PMID:Ethanol differentially regulates G proteins in neural cells. 313 33


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