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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood flow was measured in transplanted rat gliomas before and during a constant intravenous infusion of angiotensin II using hydrogen clearance methods. The brain tumor models were produced in syngeneic Wister-King-Aptekman male rats with stereotaxic inoculation of ethylnitrosourea-induced glioma cells (KEG-1). Induced hypertension up to 150 mmHg (mean arterial pressure) with the infusion of angiotensin II resulted in a significant increase of blood flow to tumor center compared to the normotensive state (p less than 0.001). Blood flow measured simultaneously in brain tissue of tumor-free contralateral hemisphere did not change. The therapeutic effect of administration of the simultaneous 1-(4-Amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) and angiotensin II was evaluated in four experimental groups with the tumor-bearing rats. Twelve days after tumor implantation, the rats were administered angiotensin II to increase the mean arterial blood pressure to 150 mmHg, followed by intravenous injection of ACNU injection. The increased blood pressure was steadily maintained for 20 minutes. The ACNU/induced hypertension group showed a median survival time of 27.0 days, which was significant longer (p less than 0.02) than that of an ACNU treatment group (22.0 days), a hypertension treatment group (19.0 days), or a no treatment group (18.5 days). The enhanced therapeutic effect can be attributed to improving chemotherapeutic drug delivery due to increased blood flow in the tumor.
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PMID:Modification of tumor blood flow and enhancement of therapeutic effect of ACNU on experimental rat gliomas with angiotensin II. 235 53

Gap junctional intercellular communication (GJIC) as measured by metabolic cooperation was examined in a rat glioma cell line P98F47. X-ray induced mutants of P98F47 cells were grown in 6-thioguanine selective medium (6TG medium) to separate 6TG-resistant HGPRT- mutant cells (6TGr). By co-culturing 200 6TGr cells with varied high densities of the wild type 6TG-sensitive cells (6TGs), it was found that the recovery of 6TGr cells depended on the density of 6TGs cells. Higher densities of 6TGs cells reduced the recovery of 6TGr cells. These results demonstrate the ability of P98F47 cells to perform metabolic cooperation which is indicative of GJIC. When metabolic cooperation was inhibited, increased recovery of 6TGr cells was observed. Presented results also demonstrate metabolic cooperation between P98F47 glioma cells and normal rat glial cells. Effect of tumor promoting chemicals on metabolic cooperation of P98F47 cells was studied. 3H-uridine nucleotide autoradiography technique was used to confirm the above observations. The results suggest that these cells may provide the basis for an in vitro assay specially to study brain tumor promoters and neurotoxins.
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PMID:Gap junctional intercellular communication (GJIC) in rat glioma cells--characterizations to detect inhibitors of metabolic cooperation. 237 72

Small animal models such as the rat have serious limitations for multiple human scale instrumentation, surgical manipulations, and computerized tomographic (CT) evaluations, so that large animal models are required for the study using them. Although brain tumors induced with Rous sarcoma virus in neonatal beagle or adult monkey had been reported, these animals are very expensive ones for tumor research. A major drawback of virally induced brain tumor model is, moreover, the need for specialized viral facilities and safety precautions for laboratory personnel. In this paper, a cat glioma model implanted with C6 glioma cells derived from rats injected with N-nitrosomethylurea is reported. For an implantation dose of 5 x 10(5) cells/50 microliters, C6 glioma cells were suspended in modified Eagle medium supplemented with 10% fetal bovine serum and 0.5% agar. Twenty adult mongrel cats were injected with 5 x 10(5) C6 glioma cells intracerebrally. Implanted cats had brain tumors of about 10 mm in diameter with a yield of 80%. The mean survival was about 3 weeks after implantation. Tumors developed as spheroidal, hemorrhagic masses with central areas of necrosis and peripheral edema. They were located within the parenchyma of the implanted region. This tumor possessed many of the histological and radiological characteristics of human glioblastoma such as the following: Areas of hemorrhage and necrosis surrounded by pseudopallisading were observed within the tumor consisting of spindle-shaped cells with pleomorphic nuclei. A mass lesion with ring or garland-like enhancement surrounded by brain edema was shown on the CT scans.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Experimental brain tumor in adult mongrel cat]. 239 Mar 66

Vasogenic brain edema was produced by transplantation of rat glioma C6 cells into rat brain. Using this model, we measured neurotransmitter concentrations and water content of regional brain tissue. In the tumor-implanted controls, monoamine neurotransmitters in the hypothalamus, cortex, and striatum significantly decreased. When treated with DEX, these monoamines tended to return to the levels of the sham-operated controls. Additionally, DEX markedly lowered tumoral monoamines. In the nonsurgical animals, DEX significantly increased norepinephrine but not DA. Regardless of treating with DEX or not, water content showed no changes in the hypothalamus and striatum in the tumor-implanted animals. However, the increase in water content in the cortex was significant, and this increase could be reduced by DEX to the levels of controls. Water content of tumor tissue could also be markedly reduced by DEX. In the nonsurgical animals, there were no changes in water content between DEX-treated and nontreated animals. In conclusion, brain edema produced by the brain tumor may reduce noradrenergic and dopaminergic activities. This is more likely due to compression anoxia caused by the tumor mass, glial hydrops, and edema fluid. It is presumed that the effect of DEX is due to reduction of water content of the tumor and peritumoral white matter as well as by increasing noradrenergic activity.
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PMID:Effect of dexamethasone on neurotransmitter amines in a rat glioma model. 239 42

Subpopulations of infiltrating lymphocytes were studied by immunohistological method using monoclonal antibodies in gliomas and metastatic brain tumors. Thirteen specimens from 8 glioma patients, and 7 specimens from 3 metastatic brain tumor patients were used. No special therapy for brain tumor had been performed in these cases, but 3 glioma patients and all metastatic brain tumor patients had received steroid hormone. Frontal lobe obtained from the autopsy case of chest trauma was served as a normal control. Frozen sections were stained with avidin-biotin peroxidase complex method using Leu-series monoclonal antibodies for pan T-cells (Leu-1), cytotoxic/suppressor T-cells (Leu-2 a), helper/inducer T-cells (Leu-3 a) and B-cells (Leu-12). Lymphocyte infiltrates were quantitated by counting positively stained cells in 13 glioma and 7 metastatic brain tumor specimens. In normal frontal lobe, only a few T-cells infiltrated around several blood vessels in the parenchyma and subarachnoid space. But in the cases of glioma, many perivascular lymphocytic infiltrates were found and in the cases of metastatic brain tumor, many lymphocytes were found diffusely in the interstitial area between nests of tumor cells. Most of these lymphocytes were T-cells and B-cells were scarce, and Leu-2 a and Leu-3 a positive cells intermingled with each other. Len-3 a/2 a ratio ranged from 0.2 to 0.9 in the half of gliomas and 1.5 to 3.6 in another half of gliomas, three of which were treated with steroid hormone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Immunohistological analysis of infiltrating lymphocyte subpopulations in gliomas and metastatic brain tumors]. 243 10

The anticancer chemotherapeutic agent cisplatin (cis-diamminedichloroplatinum) has several disadvantages, including extreme nephrotoxicity, rapid binding to plasma proteins, and poor penetration into the central nervous system. Liposomes would seem to be suitable as carriers of cisplatin to brain tumors. This ultrastructural study was undertaken to identify the capillary permeability of liposome-encapsulated cisplatin in a rat brain tumor model. Brain tumors were induced transplacentally with a single intravenous dose of 50 mg/kg of ethylnitrosourea (ENU). One ml of liposome-encapsulated cisplatin and ferritin prepared from phosphatidylcholine and cholesterol (molar ratio 7:2) was administered via the carotid artery to rats with ENU-induced brain tumors. The tumor platinum content and that of the contralateral hemisphere were assayed by flameless atomic absorption spectrometry. The presence of ferritin-bearing liposomes was demonstrated by electron microscopy of brain capillary endothelium as well as tumor cells. Thirty minutes after drug administration, the average dry-weight platinum concentrations were 3.98 +/- 0.50 micrograms/g within the intracerebral tumors and 0.72 +/- 0.24 micrograms/g in the contralateral hemispheres. Electron microscopic ultrastructural study, which can distinguish ferritin-bearing liposomes from cell materials, demonstrated the presence of liposomes containing ferritin in both cell surface folds and capillary endothelial cells and also within tumor cells. An enlarged electron micrograph of a liposome with a diameter of approximately 0.2 micron suggested the presence of ferritin molecules in the lamellar structure. Liposome-encapsulated cisplatin is apparently able to pass the blood-brain barrier and should be useful in the chemotherapy of glioma.
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PMID:[Ultrastructural study of capillary permeability of liposome-encapsulated cisplatin in an experimental rat brain tumor model]. 247 62

The inhibitory effects of 4 retinoids, namely, retinal (Ral), retinoic acid (RA), retinyl acetate (RAc), and retinyl palmitate (RP), and 3 carotenoid including beta-carotene (BCT), lycopene (LCP), and crocetin (CCT) on the growth and DNA synthesis of rat C-6 glioma cells were studied. All the retinoids and carotenoids caused reduction of plating efficiency and inhibition of the cellular growth. RA was the most potent inhibitor of plating efficiency, followed in decreasing order by RAc, Ral, LCP, RP, BCT, and CCT. The effects of various doses of retinoids and carotenoids on the inhibition of DNA synthesis were clearly demonstrated in the growing C-6 glioma cells, whereas negligible effects of these compounds on the RNA and protein synthesis were observed. These results suggested that retinoids or carotenoids are biologically active as anti-tumor agents against brain tumor cells in culture, while carotenoids appeared to be less active.
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PMID:Inhibitory effects of carotenoids and retinoids on the in vitro growth of rat C-6 glioma cells. 248 Jun 12

With the aid of interleukin 2 (IL-2), two phenotypically different cytotoxic T lymphocyte (CTL) clones were established with target specificity against syngeneic murine malignant brain tumor (a methylcholanthrene-induce ependymoblastoma of C57BL/6 mouse origin, 203-glioma). Furthermore, the cloned CTL lines were characterized in vitro, and their in vivo effectiveness was investigated by intracerebral (i.c.) tumor neutralization assay and adoptive immunotherapy with the clones for i.c. tumor-bearing mice. Each CTL clone retained an IL-2 dependency with a defined functional activity. G-CTLL 1 with a phenotype of Lyt-1-.2.3+ exhibited a target cytotoxicity against 2 kinds of murine glioma cells, syngeneic 203-glioma and allogeneic RSV-M glioma (Schmitt-Ruppin rous sarcoma virus-induced malignant astrocytoma). It is noted that G-CTLL 1 cells produced gamma interferon (IFN) by stimulation with glioma antigens. The spontaneous release of gamma IFN paralleled the amounts of exogenous IL-2 added into the cultures, but IL-2 had no synergistic effects on IFN release in the presence of tumor antigens. Furthermore, by adding anti-mouse gamma IFN antibody, the IFN production of G-CTLL 1 cells was inhibited but their lytic potential was hardly reduced in vitro. In contrast, G-CTLL 2 cells expressed a cell surface phenotype of Lyt-1+.2.3+ with more restricted target specificity against only syngeneic 203-glioma cells, although they showed a weaker cytotoxicity than G-CTLL 1 cells and no release of gamma IFN. The in vivo therapeutic efficacy using G-CTLL 1 cells was confirmed in both adoptive immunotherapy and tumor neutralization assays.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An experimental approach to specific adoptive immunotherapy for malignant brain tumors. 251 84

To ascertain whether tumor-specific immune response occurs in patients with malignant brain tumors, lymphocyte blastogenetic responses to tumor cells were examined in 18 patients prior to operation and other treatment. Among 12 patients with malignant glioma, the peripheral blood lymphocytes (PBL's) showed a positive blastogenetic response to their own glioma cells in seven (58.3%), whereas the tumor-infiltrating lymphocytes (TIL's) showed a positive response in only three (25%). In four (66.7%) of six patients with metastatic brain tumors, however, both the PBL's and TIL's showed a positive blastogenetic response to their own tumor cells. In these four patients, this lymphocyte blastogenetic response to tumor cells were at a much lower level compared with phytohemagglutinin P or allogeneic lymphocyte stimulation. Furthermore, these responses were increased when the cells were cultured with interferon-gamma (500 U). Other lymphokines had no effect on the response. This method appears to be useful in identifying the tumor-specific immune response in patients with malignant brain tumor.
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PMID:Analysis of mixed lymphocyte-tumor culture in patients with malignant brain tumor. 252 72

In Brain Tumor Cooperative Group Study 77-02, eleven institutions randomized 603 adult patients with supratentorial malignant glioma to one of four treatment groups following surgery: conventional radiotherapy (6000 cGy in 30-35 fractions) + BCNU, conventional radiotherapy + streptozotocin, hyperfractionated (twice daily) radiotherapy (6600 cGy in 60 fractions) + BCNU, and conventional radiotherapy with misonidazole followed by BCNU. Data were analyzed for the total randomized population and for the 557 patients (86% with glioblastoma multiforme) who met protocol eligibility specifications (including confirmed histopathology on central review). Median survival was approximately 10 months following randomization. Overall there was no statistically significant difference in survival among the four groups. Among non-glioblastoma patients, the misonidazole group appeared to have poor survival. Peripheral neuropathy was a dose-limiting toxicity with misonidazole. It is concluded that neither the addition of misonidazole nor hyperfractionated radiotherapy as given in this protocol offered any advantage over conventional radiotherapy plus either BCNU or streptozotocin for treatment of malignant glioma.
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PMID:Results of a randomized trial comparing BCNU plus radiotherapy, streptozotocin plus radiotherapy, BCNU plus hyperfractionated radiotherapy, and BCNU following misonidazole plus radiotherapy in the postoperative treatment of malignant glioma. 254 93


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