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)

We have reported previously that platelet-activating factor (PAF) interacts with the neuronal cell line NG108-15 (neuroblastoma X glioma hybrid) and the pheochromocytoma cell line, PC12. PAF acts on these cells by raising levels of intracellular free calcium ions. In the present report, we extend these studies. PAF induced the vesicular release of adenosine 5'-triphosphate (ATP) from PC12 cells in a dose-dependent manner. The PAF-induced ATP release was inhibited by the PAF antagonists, CV-3988 and CV-6209, and the calcium antagonist prenylamine. The relevance of the interaction of PAF with neuronal cells was investigated further by using brain synaptosomal preparations and primary cortical and neostriatal cells. Nanomolar concentrations of PAF induced calcium transients in aequorin-loaded synaptosomal preparations, and cortical and neostriatal cells were sensitive to the action of PAF. The possible physiological and pathophysiological roles of PAF in brain function are discussed.
Lipids 1991 Dec
PMID:Calcium ion mobilization in neuronal cells induced by PAF. 181 10

We used double-label quantitative autoradiography to measure blood flow (with 131I-iodoantipyrine) and blood-to-tissue transport of 14C-alpha aminoisobutyric acid, AIB) in thirteen 9L gliosarcomas transplanted intracerebrally into Fischer-344 rats. Microscopically, the typical pattern of 9L tumor growth was observed: a solid central tumor mass surrounded by extensive perivascular invasion. The averaged mean whole tumor transfer constant, K, of AIB in the 9L tumors was 33 +/- 15 (+/- SD) microliters/g/min. The averaged mean value of blood flow, F, was 72.2 +/- 27.3 ml/100 g/min. In brain around tumor (BAT), K (13 +/- 4 microliters/g/min) was lower than in the solid tumor, but was still 6-9 times that of tumor-free brain. F in BAT (115.9 +/- 64.6 ml/100 g/min) was comparable to values in tumor-free cortex in the same hemisphere. Values of K and F were used to calculate a net extraction fraction (En) for different regions of brain and tumor. The value of En of AIB in normal cortex was 0.003, in BAT En was 0.02, and in whole tumor the value was 0.09. The delivery of water-soluble compounds in 9L brain tumors is limited by the permeability/surface area characteristics of the tumor capillaries. The properties of blood-to-tissue transport and blood flow of 11 different brain tumor models are compared, and discussed with regard to the choice of brain tumor models for drug delivery research. The 9L brain tumor model is comparable to other transplanted rat brain tumor models, although the extent of tumor cell invasion into BAT makes this model distinctive. However, with regard to blood-to-tissue transport the 9L model differs from autochthonous models and transplanted human glioma models. We discuss guidelines for selecting brain tumor models with which to study the problem of drug delivery to brain tumors.
J Neurooncol 1991 Dec
PMID:Blood flow and blood-to-tissue transport in 9L gliosarcomas: the role of the brain tumor model in drug delivery research. 182 40

Several lines of evidence suggest that gangliosides may play a role in the regulation of growth in many cell types. Here we describe the effects on growth of two different cell lines by the addition of two different chemicals which have been reported to elevate the cellular ganglioside content through different mechanisms. Growth of neuroblastoma (Neuro 2a) cells in medium containing fetal bovine serum was inhibited in a dose-dependent fashion by both exogenous GM1 ganglioside and NeuAc2en, an inhibitor of sialidase activity. In contrast, growth of glioma cells (U-1242 MG) was not affected by exogenous GM1 or NeuAc2en in the presence of as little as 1% calf serum. However, NeuAc2en inhibited growth of U-1242 MG cells stimulated by platelet-derived growth factor in serum-free medium. These results demonstrate that the growth inhibitory effects of ganglioside on U-1242 MG but not Neuro 2a cells can be counteracted by serum, suggesting that the mechanisms through which gangliosides affect cell growth may be different for different growth factors and cell types.
J Neurooncol 1991 Dec
PMID:Effects of GM1 and 2-deoxy-2,3-dehydro-N-acetylneuraminic acid (NeuAc2en) on neuroblastoma (Neuro 2a) and human glioma cells (U1242 MG). 182 41

Antineoplastic effects of interferons (IFNs) on brain tumors have often been reported in the literature, however, so far as we know, there are no reports of the study on the antineoplastic effect of IFNs (alpha, beta, and gamma) labelled with fluorescein isothiocyanate (FITC) using flow cytometry (FCM). Three established glioma cell lines and 11 cultured cells of brain tumor from surgical specimens were exposed to IFN-alpha, beta, and gamma at the concentrations of 10(2)-10(5) IU/ml for 24 h, respectively. Using FCM, the viability of the cells was evaluated with fluorescein diacetate stain and the cell cycle was analyzed from the DNA-histogram with propidium iodide stain. Furthermore, FITC-labelled IFN-alpha, beta and gamma were also contacted with each cell to calculate respective positive cells. The viability decreased about 60% on day 1 and day 3, indicating the effect of IFN-alpha and beta on U373MG cells and on some cultured glioma cells from surgical materials, whereas, IFN-gamma had no effects. Antineoplastic effect of each IFN well correlated with FITC-positive rates, demonstrating S phase block in the cell cycle. IFN-gamma had no antineoplastic effects, whereas IFN-alpha and beta showed antineoplastic effects, which fact suggested that IFN-gamma receptor be different from those of IFN-alpha and beta. The method of FITC-labelling for IFNs with the aid of FCM has the advantages as follows: 1) Antineoplasticity of IFN can be simply evaluated with FCM; 2) It is easy to analyze the action mechanism of IFN; 3) Information on the receptor is obtainable; and 4) Sensitivity can be evaluated prior to administration of IFN, suggesting possibilities of clinical application of this method.
J Neurooncol 1991 Dec
PMID:Flow cytometric analysis of antineoplastic effects of interferon-alpha, beta and gamma labelled with fluorescein isothiocyanate on cultured brain tumors. 182 42

Lysis of tumor cells by activated cytotoxic lymphocytes requires their recognition of antigens associated with major histocompatibility complex molecules. The authors studied the constitutive expression of Class I and Class II major histocompatibility complex antigens on mouse brain-tumor cells and the capacity of different cytokines and cytokine combinations to alter this expression in vitro. Cells from the murine glioma 26 (GL26), glioma 261 (GL261), and ependymoblastoma A (EpA) cell lines were established in monolayer culture and treated for 48 hours with either alpha interferon, gamma interferon, tumor necrosis factor alpha, tumor necrosis factor alpha plus gamma interferon, or interleukin-2. They were then analyzed by flow cytometry for baseline and cytokine-altered major histocompatibility complex expression. All cell lines had a similar constitutive major histocompatibility complex pattern with low Class I antigen expression and no detectable Class II antigen expression. Alpha interferon substantially induced and up-regulated Class I antigen expression, but had no effect on Class II antigen expression. Gamma interferon also stimulated up-regulation of Class I antigen expression, generally doubling the anti-Class I antigen fluorescence of treated cells. Its effect on Class II antigen expression was more extensive. In the GL26 and GL261 cell lines the expression of Class II antigen determinants increased to 12 x and 14 x control values and as many as 75% of cells that had no detectable constitutive expression of Class II antigen expressed this antigen after priming with gamma interferon. The addition of tumor necrosis factor alpha to gamma interferon further increased Class II antigen expression on EpA tumor cells only. Interleukin-2 and tumor necrosis factor alpha alone had no effect on Class I or Class II antigen expression of any cell lines. It is concluded that Class I and Class II antigen expression in mouse glioma cell lines is induced and enhanced after treatment with certain cytokines in vitro. Use of these cell lines to create in situ primary brain tumors in C57BL/6 mice should provide an excellent animal system to study major histocompatibility complex modulation in brain tumor cells and to examine the potential impact of major histocompatibility complex up-regulation on the response of brain tumors to immunotherapy.
J Neurosurg 1991 Dec
PMID:Expression and modulation of major histocompatibility antigens on murine primary brain tumor in vitro. 158 18

Basic fibroblast growth factor (bFGF) is a potent mitogen and angiogenic factor. bFGF is expressed by a variety of solid human tumors and has been implicated as an autocrine regulator of tumor growth. Different solid tumor lines including glioma, colon carcinoma and melanoma were examined for intracellular immunoreactive bFGF, high- and low-affinity bFGF receptors and mitogenic response to bFGF when grown in chemically defined medium. All tumor lines contained significant levels of bFGF. In addition, all tumor lines contained subsets of five forms of immunoreactive bFGF, as well as 0.68-20 x 10(6) low affinity bFGF binding sites (Kd = 15-300 nM). Most, but not all lines exhibited high affinity bFGF receptors (Kd = 25-40 pM). Glioma cell lines were distinguished by expressing the highest levels of bFGF protein as well as the most high-affinity receptors for bFGF. Furthermore, glioma cell lines were the only tumor type mitogenically responsive to bFGF. These results indicate that glioma cells express high levels of this potent mitogen and angiogenic factor relative to human colon carcinoma and melanoma cells. The expression of bFGF and bFGF receptors by glioma cells may be related to abnormal growth and neoplastic progression in these tumors.
J Neurosci Res 1990 Dec
PMID:Basic fibroblast growth factor: a potential autocrine regulator of human glioma cell growth. 196 81

The uptake of glutamate in rat glioma C-6 cells and cultured astrocytes derived from rat cerebral hemispheres was found to be mediated by a Na(+)-dependent and a Na(+)-independent system. The Na(+)-dependent system was inhibited by aspartate and was consistent with the commonly occurring system designated system X-AG. The Na(+)-independent system was inhibited by cystine and was consistent with system x-c described in various types of cells in the periphery. It was also found that quisqualate selectively and competitively interfered with the Na(+)-independent glutamate uptake. In C-6 cells, the glutamate uptake via systems X-AG and x-c accounted for approximately 35% and 55% of the total uptake, respectively, at 0.05 mM glutamate. In cultured astrocytes, the glutamate uptake via system X-AG was very potent, whereas the uptake via system xc- was relatively weak and its contribution to the total uptake of glutamate seemed almost negligible. However, in both C-6 cells and astrocytes, system xc- was necessary for the uptake of cystine, another substrate of system xc-. Cystine in the culture medium was an essential precursor of glutathione, and the inhibition of the cystine uptake by excess glutamate as a competitor led to a severe deficiency in glutathione, followed by cell degeneration.
J Neurochem 1990 Dec
PMID:Uptake of glutamate and cysteine in C-6 glioma cells and in cultured astrocytes. 197 89

We present interim survival data for a group of 83 adult patients with recurrent malignant glioma treated by implanting stimulated autologous lymphocytes into the tumour bed following surgical debulking. The patients were treated 6 months or more prior to data analysis. Fifty-nine patients were male and 24 female. The mean age for the entire group was 48.4 years and the mean Karnofsky rating (KR) was 67.2. Eight of the patients had grade II tumours, 33 had grade III tumours and 42 had grade IV tumours. Statistical analysis focuses on tumour grade, KR and patient age, factors that have been shown to affect survival in previous studies. Multifactorial analyses are employed to identify interrelationships among factors related to survival. Seven patients (8%) did not respond to immunotherapy, 76 (92%) had a good initial response. Twenty-five patients (30.1%) are living and 18 (22%) have shown no evidence of recurrence. Results are evaluated in the light of those obtained in trials of other experimental therapies for recurrent malignant gliomas. It is concluded that the present protocol offers a safe and comparatively effective treatment option.
Neurol Res 1990 Dec
PMID:Immunotherapy for recurrent malignant glioma: an interim report on survival. 198 72

FK973, a novel antitumor antibiotic, was obtained as a fermentation product of Streptomyces sandaensis. FK973 had excellent cytotoxic effects against in vitro cultured human glioblastomas, medulloblastomas, and murine glioma (203 glioma) cells. The antitumor effects were also well observed against ACNU resistant glioma cells. FK973 did not go through the blood-brain barrier. The median survival time (MST) of MG models treated with FK973 was 21 days. On the other hand, the MST of the control group was 15 days. In the in vitro assessment against neural disturbance, FK973 showed a little disturbance of murine brain cells but less toxic than ADM. In the in vivo neurotoxicity examination, FK973 showed no clear damage to the neural cells and myelin sheaths.
Nihon Gan Chiryo Gakkai Shi 1990 Dec 20
PMID:[Antitumor activity of FK973 for malignant gliomas and its assessment for normal brain cells]. 207 87

Transferrin (TF), a major plasma protein, binds and transports ferric iron. Evidence exists for unique roles for TF in brain in oligodendrocyte differentiation, myelination and neuronal development. In this study, 5' flanking regions of the TF gene important in regulating gene expression were identified by transfected cell studies and a comparison of 5' flanking sequences of the human TF and TF receptor genes. Human glioma cell lines HTB-16 and HTB-17 were shown to synthesize TF identical in size and immunological reaction to TF synthesized by liver. The expression of a series of human chimeric TF genes in glioma cells was compared with hepatoma and HeLa cells. A difference in transient expression was observed in hepatoma and glioma cells transfected with TF chimeric genes containing 3.9 kb of the 5' region; hepatoma cells demonstrated significantly more expression than did glioma cells, suggesting that a DNA region present in the 3.9-kb construct is important either in liver-specific expression or in repression of brain expression, or in both. Smaller constructs containing less than or equal to 0.622 kb of the 5' regulatory region of the TF gene failed to demonstrate cell-specific expression; they were expressed in HeLa cells, a line that does not synthesize TF. High levels of expression of 0.15-kb TF constructs were also observed in hepatoma and glioma cell lines, but not in transgenic mice. Possible explanations of differences observed in expression of shorter TF constructs in vitro and in vivo are discussed.
J Neurosci Res 1990 Dec
PMID:Expression of chimeric human transferrin genes in vitro. 207 22


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