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 composition of the free amino acid pools in various brain tumors and in normal brains obtained at surgery or at autopsy is determined with an automatic amino acid analyzer and the results statistically evaluated. The tumors have lower ratios of GABA in the pools than the normal brain; tumors with higher GABA ratios are found in those which are in close contact with and have an invasive nature to brain tissue. In gliomas, the more malignant a tumor becomes, the more different the composition in that tumor is from that in normal brain tissue. But conversely, the ratio of GABA is highest in glioblastoma. The composition of the pool in oligodendroglioma is not significantly different from that in the normal brain. Metastatic brain tumors show the highest ratios of phenylalanine, tyrosine and methionine in the pool among the tumors and the normal brain. From the viewpoint of the composition of the free amino acid pools, like from that of the histological aspects, brain tumors seem to be classified into four groups: glioma, neurinoma, meningioma and metastatic tumors.
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PMID:Composition of free amino acids in brain tumors. 54 90

Incubation of neuroblastoma X glioma hybrid cells for 12-97 hr with methionine-enkephalin results in an increase in adenylate cyclase activity [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] that is mediated by the opiate receptor. The results show that cells become tolerant to, and dependent upon, enkephalin.
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PMID:Tolerance and dependence evoked by an endogenous opiate peptide. 106 10

In order to evaluate the methionine uptake of a glioma with positron emission tomography (PET), the kinetics of carbon-11 methionine was investigated in 11 patients by measuring the free 11C-methionine in plasma as an input function following intravenous administration. When the mean clearance curve of free 11C-methionine in plasma instead of individual 11C-methionine clearance curves was used, mean differences in uptake rate and distribution volume were 4.0% and 4.6% respectively. By applying the mean clearance curve of free 11C-methionine in 18 glioma patients, significant differences in 11C-methionine uptake rate and distribution volume were found according to pathological grading. For the accurate evaluation of the metabolism of 11C-methionine, it is therefore preferable that the actual level of free 11C-methionine in the plasma be measured, especially for the follow-up of individual cases. The study also demonstrated that the mean clearance curve of 11C-methionine in plasma might be employed as an input curve for calculating the uptake rate and distribution volume with small errors.
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PMID:Dynamic study of methionine uptake in glioma using positron emission tomography. 131 5

To shed light on the metabolic changes in glioma following therapy, uptake changes among 18F-fluoro-2'-deoxyuridine (18FUdR), 14C-thymidine (dThd), 14C-methionine (Met) and 3H-deoxyglucose (DG) in glioma model after chemotherapy were studied, as a means for interpreting clinical PET results, together with the changes in the bromodeoxyuridine (BUdR) labeling index. 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(-2chloroethyl)-3-nitro sourea hydrochloride (ACNU) was administered intraperitoneally in the tumor-bearing rats and uptake of the tracers or BUdR labeling index in tumor tissue were measured. The metabolic response following chemotherapy was a sharp fall immediately for 14C-dThd and 18FUdR and a moderate fall for 14C-Met whereas there was a fall in 3H-DG from 1 week after chemotherapy. The changes of BUdR labeling index paralleled that in the uptake for dThd and FUdR. These result indicate that PET scans using a variety of tracers in conjunction could be used for clinical diagnosis and evaluation of therapy in glioma cases. 18FUdR is a promising tracer of nucleic acid metabolism to evaluate the proliferative potential of brain gliomas.
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PMID:Metabolic changes of glioma following chemotherapy: an experimental study using four PET tracers. 146 67

Nitrous oxide irreversibly inactivates cob(I)alamin, which serves as a cofactor of the enzyme methionine synthase catalyzing the remethylation of homocysteine to methionine. In patients exposed to nitrous oxide, increase in plasma homocysteine is a responsive indicator of cob(I)alamin inactivation. In the present work, we measured the inactivation of methionine synthase and the concurrent homocysteine export rate of two murine and four human cell lines during nitrous oxide exposure. When cultured in a standard medium with high content (2.3 microM) of folic acid, the methionine synthase of all cell types was inactivated at an initial rate of 0.05 to 0.14 h-1. The inactivation curves leveled off, and a residual activity of 15 to 45% was observed after 48 h of nitrous oxide exposure. The rate and extent of the nitrous oxide-induced inactivation were markedly reduced when the cells were transferred and cultured (greater than 10 days) in a medium containing low concentration (10 nM) of 5-methyltetrahydrofolate. The methionine synthase inactivation increased in a dose-dependent manner when the 5-methyltetrahydrofolate content of the medium was increased from 3 nM to 2.3 microM. The inactivation of methionine synthase was associated with a marked enhancement of homocysteine export rate of murine fibroblasts and a moderate increase in export from two human glioma cell lines. In contrast, in three leukemic cell lines (murine T-lymphoma R 1.1 cells, human promyelocytic leukemia HL-60 cells and human acute myelogenous leukemia KG-1a cells), the homocysteine export rates were not increased during nitrous oxide exposure. In the responsive murine fibroblasts and the glioma cells, the homocysteine export rate varied inversely to the changes in methionine synthase activity induced by nitrous oxide exposure at different concentrations of folate in the medium. The enhancement of homocysteine export rate of some cell types during nitrous oxide exposure probably reflects inhibition of homocysteine remethylation in intact cells, and highlights the utility of extracellular homocysteine as an indicator of metabolic flux through the methionine synthase pathway. No enhancement of homocysteine export despite inactivation of methionine synthase in three leukemic cell lines questions the functional state of the enzyme in these cells.
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PMID:Homocysteine remethylation during nitrous oxide exposure of cells cultured in media containing various concentrations of folates. 160 76

After exposure to low density lipoprotein (LDL) that had been minimally modified by oxidation (MM-LDL), human endothelial cells (EC) and smooth muscle cells (SMC) cultured separately or together produced 2- to 3-fold more monocyte chemotactic activity than did control cells or cells exposed to freshly isolated LDL. This increase in monocyte chemotactic activity was paralleled by increases in mRNA levels for a monocyte chemotactic protein 1 (MCP-1) that is constitutively produced by the human glioma U-105MG cell line. Antibody that had been prepared against cultured baboon smooth muscle cell chemotactic factor (anti-SMCF) did not inhibit monocyte migration induced by the potent bacterial chemotactic factor f-Met-Leu-Phe. However, anti-SMCF completely inhibited the monocyte chemotactic activity found in the media of U-105MG cells, EC, and SMC before and after exposure to MM-LDL. Moreover, monocyte migration into the subendothelial space of a coculture of EC and SMC that had been exposed to MM-LDL was completely inhibited by anti-SMCF. Anti-SMCF specifically immunoprecipitated 10-kDa and 12.5-kDa proteins from EC. Incorporation of [35S]methionine into the immunoprecipitated proteins paralleled the monocyte chemotactic activity found in the medium of MM-LDL stimulated EC and the levels of MCP-1 mRNA found in the EC. We conclude that (i) SMCF is in fact MCP-1 and (ii) MCP-1 is induced by MM-LDL.
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PMID:Minimally modified low density lipoprotein induces monocyte chemotactic protein 1 in human endothelial cells and smooth muscle cells. 169 10

C6 rat glioma cells incubated in serum-free medium with D-[14C]glucosamine secrete, on stimulation with nerve growth factor (NGF) or monosialogangliosides (MSGs), several glycoproteins (Gps), the most prominent of which are a 270-, 220-, and 69-kDa Gp. Several growth factors, hormones, phorbol ester, and disialo- and trisialogangliosides did not stimulate secretion. Western blot analysis of the conditioned medium from C6 cells stimulated with NGF or MSG identified one distinct band of approximately 220 kDa for fibronectin and J1/tenascin, which comigrated. Antiserum to NGF prevented NGF-stimulated release and also blocked MSG-evoked release. The 220-kDa band was labeled after pulse labeling with [35S]methionine in the presence of NGF, and by a 15-min chase period radioactively labeled J1/tenascin could be immunoprecipitated. Tunicamycin drastically inhibited almost completely release of the 220-kDa Gp labeled by D-[14C]glucosamine or [35S]methionine. These results extend the range of neurotrophic properties attributed to NGF to cells of glial origin and suggest that NGF regulates secretion of extracellular matrix proteins. MSG stimulation of fibronectin and J1/tenascin secretion may be mediated by NGF or an NGF-like molecule also secreted by the C6 glioma cells.
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PMID:Nerve growth factor mediates monosialoganglioside-induced release of fibronectin and J1/tenascin from C6 glioma cells. 170 27

Human glioma (U-343 MGa) and human colon carcinoma (HT-29) cell lines were cultured as multicellular spheroids, and the accumulations of the L- and D-enantiomers of 11C-methionine were investigated. The accumulation of radioactivity in the spheroids was expressed as relative counts, by dividing the radioactivity measured in the spheroid with the radioactivity of the same volume of the incubation medium. The experiments were verified using 14C-labeled L- and D-methionine. The influence of spheroid volume, specific activity, incubation time, washing time, and the environmental temperatures were investigated. The spheroid model was used to determine the effect of the lipoxygenase inhibitors BW A4C and AA-861, the ether-phospholipid type PAF-antagonist CV-6209 and the protein synthesis inhibitor cycloheximide on methionine uptake. The results showed that 11C-L-methionine can be applied in the study of drug effects on multicellular tumor cell aggregates.
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PMID:Application of (methyl-11C)-methionine in the multicellular spheroid system. 174 12

Cell lines of human glioma (U-343 MGa and U-251 MG) and human glia (U-533 CG) origin were cultured as monolayers and exposed to CV-6209, an alkyl-phospholipid analog and antagonist of platelet activating factor. This drug had very potent antiproliferative effects on the studied human glioma cell lines; IC50 was 0.9 microM after 48 h treatment and 0.2 microM after 2 weeks treatment. At these doses no growth inhibitory effect was noted on the normal glia cells. The effects on the glioma cells were reversible in the dose intervals, where cell proliferation, 3H-thymidine and 14C-methionine uptakes were greatly inhibited. The simultaneous administration of platelet activating factor [(R)PAF] did not influence the antiproliferative effects of CV-6209 on the cells cultured as monolayers. The structurally similar analog CV-3988 also had antiproliferative effects, although at 10 times higher concentration than CV-6209. Two other, structurally unrelated, PAF-antagonists (WEB-2086 and TCV-309) gave effects only at very high concentrations. The U-343 MGa cell line was also exposed to CV-6209 when growing as multicellular spheroids. The studies on the spheroid cultures also demonstrated good antitumoral effects with decreases of both the volume growth and the thymidine uptake. The simultaneous administration of (R)PAF reversed the inhibitory effect of CV-6209 on thymidine incorporation. This study demonstrates a strong antitumoral effect at low concentrations of CV-6209. The antiproliferative effects were probably primarily related to the ether-lipid structure and not to the PAF-antagonistic properties. The good antitumoral effect of CV-6209 on both monolayer and spheroid cultures and the possible PAF-antagonistic properties are discussed.
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PMID:Effects of the PAF-analog and -antagonist CV-6209 on cultured human glioma cell lines. 188 7

A case of adult pilocytic astrocytoma in the right temporal lobe is reported here. The patient was a twenty-four year old man, who came to the neurological division of our hospital on October 6, 1987 because of repeated consciousness-loss attacks accompanied with uncinate fit. He had no neurological deficits. However, an EEG revealed spike-and-wave complexes in the right temporal region, and a CT scan showed a small cystic lesion in the right temporal lobe. A diagnosis of psychomotor seizure was made, and the administration of anticonvulsants was started. The incidence of attack then decreased, but after approximately two years of drug therapy the attacks increased again. A CT scan was again performed, and revealed that the lesion in the right temporal lobe was enlarging. Also a noticeable enhanced lesion, identified as a mural nodule was found in the post-contrast enhancement study. A brain tumor was then suspected, and he was admitted to the neurosurgical division on October 11, 1989. He had no neurological deficits on admission. An MRI showed a low intensity lesion in the T1 weighted image, and a high intensity lesion in the T2 weighted image. A cystic lesion with a marked enhanced mural nodule was also found in the base of the right temporal lobe, according to the Gd enhancement study. Perifocal edema was not recognized. Cerebral angiography showed no positive findings. Positron emission tomography (PET), using H2(15)O, revealed low perfusion at or around the lesion, and PET using [11C]-methionine revealed an accumulation of methionine at the lesion. A diagnosis of low-grade glioma was made, and a right temporal craniotomy, for the purpose of totally removing the tumor was performed on October 26, 1989.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of adult pilocytic astrocytoma in the right temporal lobe]. 189 Oct 62


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