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)

Xenograft intracerebral glioma models have been developed in normal mice by growing the rat C6 glioma in either adult or neonatal mouse brains. Using this tumor line it was possible to grow discrete intracerebral gliomas in either CBA or AKR adult mice or neonatal mice. The size of the tumor mass and length of survival was directly related to the number of tumor cells injected and the time after implantation. To obtain localized intracranial tumor growth cells were suspended in a 1% agarose solution before implantation. Following injection of 10(6) cells into the frontal lobe of adult CBA or AKR mice, discrete tumor masses greater than 4 mm in diameter were obtained in 90% of animals at 14 days, and the largest tumors in adult mice occurred between 21 and 28 days after implantation. The tumor size following implantation of 10(6) cells was significantly greater than with 10(5) cells at 7 days (P less than 0.05) and at 14 and 21 days (P less than 0.01). Less than 60% of mice of BALB/c, RIII, or C57 black strains developed tumors greater than 4 mm diameter at 14 days after intracerebral injection of 10(6) C6 cells. Using neonatal mice it was found that when 10(5) cells were injected intracranially tumors greater than 4 mm in diameter developed in 14 of 15 animals within 2 weeks (CBA mice). Similar results were seen in the RIII, AKR, C57 black, and BALB/c strains. Longer growth periods resulted in larger tumors, up to 8 mm in diameter (6 of 10 animals at 20 days). The tumors in the neonatal animals were not as discrete as in the adult mice, and tumor often spread to the meninges and into the lateral ventricles. The tumor harvested from the brain had a cloning efficiency of 1.2 +/- 0.4% (SD). A panel of monoclonal antibodies was raised to the C6 glioma, and this was used to define clearly the margins of the tumor within the brain. The xenograft mouse models should prove useful for the study of the therapy of gliomas.
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PMID:Development of a xenograft glioma model in mouse brain. 394 1

5-Fluorocytosine (5-FC) lacks antineoplastic activity in human subjects because of the absence of cytosine deaminase (CDase) in mammalian cells. Intratumoral conversion of 5-FC into 5-fluorouracil (5-FUra) by locally implanted capsules containing CDase followed by systemic administration of 5-FC can be expected to induce antineoplastic activity at a local site with minimal systemic toxicity. In vitro and in vivo experiments were performed to evaluate this hypothesis. Spectrophotometric analysis confirmed the deamination of 5-FC to 5-FUra by CDase extracted from cultivated Escherichia coli. In vitro studies showed that 5-FC combined with CDase induced significant growth-inhibitory effects on the cultured glioma cells. An active CDase capsule, made of cellulose tubing, was newly designed for local implantation. 5-FC concentrations in the s.c. tumors of the rats given these CDase capsules, followed by 5-FC administration, showed a sufficient amount of delivery of 5-FC to the tumor tissue. 5-FUra appearing in the tumor reached the level of 8.0 micrograms/g at 2 h and stayed at more than 1.0 microgram/g at between 1 and 6 h. Significant reduction of the tumor growth and cytotoxic changes were observed. The passive cutaneous anaphylaxis reaction demonstrated no allergic reaction to the host due to the capsule. These results suggest that this chemotherapeutic method is effective for human brain tumors.
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PMID:Antineoplastic effects in rats of 5-fluorocytosine in combination with cytosine deaminase capsules. 397 37

The energy metabolism of living tumors in rats and hamsters were investigated by obtaining in vivo 31P-NMR spectra, and the effects of chemotherapy on tumors were evaluated by observing the changes of these spectra. Tumor cells of rat glioma, human glioblastoma and human neuroblastoma were inoculated subcutaneously in the lumbar region of the animals. After the tumor grew to over 1.5 cm in diameter, in vivo 31P-NMR spectrum data was obtained selectively from the tumor with a TMR-32 spectrometer (Oxford Research Systems, U.K.). Several peaks (ATP, inorganic phosphate (Pi), phosphodiesters and phosphomonoesters (PME) were observed in the tumors. The heights of these peaks varied widely corresponding to the tumor growth. However, the spectrum pattern of each tumor in an active stage was found to be essentially the same regardless of histological type or tumor origin. The phosphocreatine (PCr) peak was small, ATP and PME peaks were large and tissue pH calculated from the chemical shift of Pi was low in each tumor group. After intravenous injection of a large dose of a chemotherapeutic agent, ATP peaks decreased and the Pi peak increased gradually, resulting in a dominant Pi peak pattern after several hours in all groups. With lower drug doses, spectrum changes were temporarily seen in the tumors. These findings indicated that drugs with a high dose have a selective and a direct action on the energy metabolism of tumor tissues. In vivo 31P-NMR spectra measurement is very valuable not only to investigate the energy metabolism in tumor tissue but also to evaluate the effects of chemotherapy on the tumor.
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PMID:Observations of energy metabolism in neuroectodermal tumors using in vivo 31P-NMR. 403 75

Mouse interferon (IFN) induced in L 929 cells by Newcastle disease virus was examined for its effect on the growth of mouse brain tumor cell line. In this study, we used subcutaneously transplanted 203 Glioma model, which had been originally induced by methylcholanthrene in C 57 BL mice. After subcutaneous transplantation, intraperitoneal administration of IFN was started by following schedule; 5 X 10(3) IU twice a week, 5 X 10(4) IU twice a week, 2.5 X 10(5) IU twice a week, 5 X 10(3) IU every day and 2.5 X 10(4) IU every day. In all groups treated by IFN intraperitoneally, no inhibition of the tumor growth was seen. On the other hand, natural killer (NK) activity was augmented by IFN treatment. Therefore, we considered that augmentation of NK activity was not directly correlated with the antitumor effect of IFN. Then, local administration was examined. After subcutaneous tumor was recognized, 2.5 X 10(4) IU of IFN was injected intratumorally every day. About 20 days later, the tumor decreased its size less than that treated by local injection of saline. It was suggested that the local administration of IFN might be better than the systemic administration.
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PMID:[Effect of interferon on mouse glioma]. 619 81

In vitro sensitivity test of cultured human malignant glioma cells to ACNU[1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride] was performed on Falcon 3064 microtestplate. Early culture cells established from 10 clinical cases were examined by means of this method and the correlation between in vitro response and clinical response of tumor to ACNU was studied. In microtestplate assay, it was defined as ACNU sensitive when the tumor growth showed more than 60% suppression when tumor was cultured in the medium which contained 40 meg/ml of ACNU. Clinical responses were evaluated by means of CT scan, being divided into 4 classes, PR (partial response), CR (complete response), NC (no change) and PD (progressive disease). The former two groups were regarded as responder and the latter two as nonresponder. The correlationship between in vitro response and clinical response was higher in resistant group (100%) than in the sensitive group (60%), so the resistant tumor can be checked with this method. For this reason, the use of this assay may prove helpful in the selection of the chemotherapeutic agents.
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PMID:[Anti-tumor activity of ACNU against malignant glioma--a clinical application of in vitro sensitivity test of chemotherapeutic agent]. 630 97

The authors studied the effect of one of the thymus preparations, thymostimulin, on the growth of experimental cerebral glioma. It was found that independent administration of thymostimulin at the beginning or in the second half of the latent period of tumor growth had no essential effect on the survival of rats. Injection of thymostimulin during chemotherapy with fluorafur increased the survival of rats considerably, both in early and in late immunotherapy.
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PMID:[Efficacy of thymostimulin in experimental combined therapy of malignant gliomas]. 642 65

Experimental models of meningeal gliomatosis (MG) have been produced by intracisternal inoculation of C6 glioma and 9L glioma cells into Wistar and Fisher 344 rats, respectively. The tumor growth was steady and fast in both MG models if 10(6) cells were implanted. Median survival time(MST) of rats inoculated with tumor cells was inversely related to the number of cells inoculated. The clinicopathological features observed in both MG models were similar to those seen in diffuse leptomeningeal involvement of gliomas in human beings. The models will be useful for investigating the pathophysiology of meningeal gliomatosis and the efficacy of chemotherapeutic agents.
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PMID:[Meningeal gliomatosis: development of experimental models]. 650 51

The polyamine metabolism of transplanted N-nitrosomethylurea-derived rat glioma was determined with radiolabeled putrescine used as a marker for malignancy. The uptake of putrescine in vivo was complete within 5 minutes and was specific for tumor tissue. The conversion of putrescine to spermine and other metabolites by the tumor was rapid, in contrast to the case for adjacent normal brain. These results suggest that putrescine labeled with carbon-11 may be used as a positron-emission tomographic tracer for the selective metabolic imaging of brain tumor and may be used in an appropriate model as a marker for tumor growth rate.
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PMID:Labeled putrescine as a probe in brain tumors. 660 20

Immunological responses to an experimental brain tumor of mice [the 20-methylcholanthrene-induced malignant glioma, 203-glioma)] were investigated. The killer T-cell activity of spleen cells, which was specific against 203-glioma cells, began to be severely impaired 2 weeks after intracranial inoculation; this impairment was concurrent with increased intracranial pressure, which was due to developing tumor growth. On the other hand, the killer T-cell activity continued for over 4 weeks in mice inoculated with the mitomycin C-treated tumor cells. Surface marker analysis showed that Lyt-1-2,3+ killer T-cells were predominant in intracranial tumor-bearing mice, whereas both Lyt-1-,2,3+ and Lyt-1+,2,3+ killer T-cells were equally present in s.c. tumor-bearing mice. The effects of adult thymectomy on the immune responses against 203-glioma were also investigated in intracranial and s.c. tumor-bearing mice. In both the intracranially and s.c. inoculated groups, killer T-cell activity was increased in mice thymectomized before 3 weeks and decreased in mice thymectomized before 10 weeks. In these mice, Lyt-1+,2,3+ killer T-cells were not detected, which suggests strongly that the progenitors of Lyt-1+,2,3+ killer T-cells are short-lived lymphocytes in contrast to those of Lyt-1-,2,3+ killer T-cells, which survive more than 10 weeks after adult thymectomy.
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PMID:Characteristic immunological responses to an experimental mouse brain tumor. 660 2

The efficacy of glioma-specific cytotoxic T-lymphocyte for a syngeneic murine malignant glioma (a 20-methylcholanthrene-induced ependymoblastoma, 203-glioma) was investigated. The cytotoxic clone (G-CTLL 1), established and expanded exponentially by T-cell growth factor, has retained target specificity for more than 6 months. In adoptive therapy and Winn assay, the in vivo antitumor activity of G-CTLL 1 was demonstrated against mice inoculated intracranially with 203-glioma cells. The therapeutic effects in adoptive immunotherapy were largely dependent on dose and time of i.v. administration, although the therapy was rather ineffective in condition of increased intracranial pressure due to the tumor growth. The mechanisms responsible for the in vivo protection were probably related to the killing activity of G-CTLL 1 or the tumor-specific production of immune interferon by G-CTLL 1.
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PMID:Specific adoptive immunotherapy with tumor-specific cytotoxic T-lymphocyte clone for murine malignant gliomas. 660 88


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