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)

Experimental animal models resembling most human brain tumor types can be induced by exposure to oncogenic viruses or chemical carcinogens: Astrocytomas and glioblastoma multiforme can be produced experimentally by intracerebral injection of oncornaviruses, whereas medulloblastomas, choroid plexus papillomas, and ependymomas can be induced by the papovaviruses. Adenoviruses have been utilized to cause medulloepitheliomas, neuroblastomas, and retinoblastomas. All three groups of viruses can result in sarcoma production. Gliomas represent the primary tumor type induced in the brain by chemical carcinogens. These autochthonous tumor systems are reviewed, with emphasis on methods, tumor type, latency period, advantages, and disadvantages. In addition, recent investigations of molecular events involved in neoplastic transformation by chemical carcinogens are summarized.
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PMID:Chemical- and virus-induced brain tumors. 20 37

Gliomas, derived from astrocytes, oligodendroglia, or ependyma, are each united into a continuum by a graduation of anaplasia. Neoplasms originate at all levels of each continuum; subsequently, some move along its declivity. Conversely, neuroblastic tumors may differentiate, whereas concomitantly in the same lesion, the glial stroma may dedifferentiate. Anaplastic glia, as in a glioblastoma multiforme, can initiate malignant transformation in alien cells.
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PMID:Nomenclature for gliomas. 20 38

Neuroblastoma x glioma NG108-15 hybrid cells exposed to N6, O2'-dibutyryladenosine 3':5'-cyclic monophosphate for several days release [3H]acetylcholine in response to serotonin, prostaglandin F2alpha, KCl, or veratridine. NG108-15 cells grown in the absence of dibutyrul cyclic AMP do not respond to an excitatory stimulus by releasing [3H]acetylcholine but can be shifted to a responsive state by treatment with dibutyryl cyclic AMP. Thus, the reactions that are required for acetylcholine release can be regulated in NG108-15 cells, thereby regulating the ability of cells to form synapses and the efficiency of synaptic communication.
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PMID:Regulation of acetylcholine release from neuroblastoma x glioma hybrid cells. 20 94

Etiology and pathogenesis of empty cella syndrome remains undetermined in some cases (primary or idiopathic type), while in others it is related to treatment of pituitary and parasellar disease (secondary type). Ten patients with empty sellae, secondary to treatment of pituitary adenomas (five cases), granulomas (three cases), craniopharyngioma (one case), and optic glioma (one case) are presented. Pathogenesis of empty sella is discussed and the importance of neuroradiologic evaluation of this syndrome is stressed.
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PMID:Secondary empty sella syndrome. 20 13

Cyclic AMP efflux was measured following hormonal stimulation of adenylate cyclase in a variety of animal cells including C-6 rat glioma cells, WI-38 human fibroblasts, and avian erythrocytes. Using a variety inhibitors of mitochondrial function and glycolysis, a correlation was noted between cellular ATP levels and the rate of cyclic AMP efflux in all cells examined. A relationship between the efflux rate and the magnitude of the membrane potential was not observed. Pharmacological agents which inhibited cyclic AMP egress in these cells without reducing ATP levels included several prostaglandins (A greater than B greater than E greater than F) and probenecid. The characteristics of the cyclic AMP efflux system resemble those of the organic anion transport system.
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PMID:Regulation of adenosine 3':5'-monophosphate efflux from animal cells. 20 41

The development of (Na+ + K+) ATPase, carbonic anhydrase and HCO3--stimulated ATPase activity was studied in developing rat brain in vivo, and in primary astrocyte cultures from 1--3-day-old rat brain as a function of increasing cell growth. The primary cultures showed an increase in all the above enzyme activities during cell growth, with time courses which were qualitatively similar to their development in vivo. Cell cultures grown separately from the cerebellum plus brain stem regions showed greater carbonic anhydrase activity than cerebral cultures over the entire 4-week growth period, corresponding to development of this activity in these same regions in vivo, HCO3-stimulated ATPase activity was slightly greater in cerebellar cultures and (Na+ + K+) ATPase activity was greater in cerebral cultures up to the second week of growth, resembling development of the same enzyme activities in vivo. C6 glioma and neuroblastoma cells showed no and 10-fold lower carbonic anhydrase activities respectively, compared to the primary astrocyte cultures. Addition of 1 mM N6-2'-O-dibutyryladenosine-3',5'-monophosphate (DBcAMP) in the presence of serum caused marked formation of cellular processes and increased carbonic anhydrase and (Na+ + K+) ATPase activity. Maximum effects were found 2 h after addition of 1 mM DBcAMP and thereafter declined. In the absence of serum such effects persisted for at least 24 h. Electron microscope studies showed large numbers of microtubule (approximately 20 nm diameter) and filamentous structures (less than or equal to 10 nm diameter) in the cytoplasm, which showed changes in distribution in cells treated with DBcAMP. This study suggests that the increase in ATPase and carbonic anhydrase activities in rat brain with increasing age may be in part a reflection of proliferation and development of astroglia cells. Together with the morphological data, it also provides additional evidence that primary cultures derived from neonatal rats may closely resemble developing astroglia in vivo.
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PMID:Enzymatic and morphological properties of primary rat brain astrocyte cultures, and enzyme development in vivo. 20 76

Brain tumors were induced in Syrian hamsters by intracerebral inoculation of brain cells which were obtained from 12-day old syngeneic hamster and infected with Schmidt-Ruppin strain of Rous sarcoma virus (SR-RSV) in vitro. A total of 212 tumors were developed in all 25 recipients within 19 to 125 days after transplantation. On the basis of light and electron microscopic study, they were classified into four main groups: astrocytoma (45.8%), pleomorphic glioma (50.0%), sarcoma (3.8%), unclassified (0.4%). The morphological features of these tumors were described, and the advantages of this brain tumor model were discussed.
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PMID:Brain tumors induced in hamsters by intracerebral inoculation of SR-RSV-infected embryonic brain cells. 21 Jun 20

Mouse neuroblastoma clonal cell line N4TG1 has 20,000 enkephaline (opiate) receptor binding sites/cell, but contains undetectable levels of sulfogalactosylceramide as judged by quantitative and isotope-labeling studies. Mouse glioma cell lines G26-20 and G26-24 contain substantial quantities of sulfogalactosylceramide, but do not bind enkephalins. Preincubation of cells with sulfogalactosylceramide or other anionic glycosphingolipids did not enhance or induce opiate receptors. Thus, sulfogalactosylceramide is not an integral part of the opiate receptor of N4TG1 cells.
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PMID:Evidence for the noninvolvement of sulfogalactosylceramide (cerebroside sulfate) in the enkephalin (opiate) receptor. 21 24

C6 glioma cells and B104 neuroblastoma cells both possess adenylate cyclase activity, but only C6 cells have beta-adrenergic receptors. However, when cocultured with B104 cells, C6 cells show a marked decrease in their ability to accumulate adenosine 3', 5'-monophosphate upon stimulation with beta receptor agonists. Since both beta receptors and cholera toxin-stimulated adenylate cyclase activities are present in C6/B104 cocultures, we conclude that the beta receptor/adenylate cyclase transduction mechanism in cocultured C6 cells is uncoupled.
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PMID:Cellular interactions uncouple beta-adrenergic receptors from adenylate cyclase. 21 32

The clinicopathologic features of eight new cases of combined intracranial sarcoma and glioma are described. This type of mixed cerebral tumor is histologically characterized by a peripheral distribution of the gliomatous elements in relation to a more centrally situated meningeal or intracerebral sarcoma, and by the frequent presence of gradual transitions from reactive to frankly neoplastic astrocytes. In six of the eight cases, the additional development of either infiltrating astrocytoma or frank glioblastoma in the adjacent brain was demonstrated; this was interpreted as a further expression of malignant glial reaction. It is suggested that these tumors be termed "sarcogliomas" to distinguish them from the type of mixed glioma and sarcoma that has recently been redesignated "gliosarcoma."
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PMID:Reactive glioma in intracranial sarcoma: a form of mixed sarcoma and glioma ("sarcoglioma"): report of eight cases. 21 76


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