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)

Sixteen pediatric patients with brainstem glioma were treated with a combination of interferon-beta, 1-(4-amino-2-methyl-5-pyrimidinyl)-methyl-3-(2-chloroethyl)-3-nitroso ure a hydrochloride (ACNU), and radiation therapy (IAR therapy). All patients received 1-1.5 million IU/day of interferon-beta intravenously for 1 week of each 6-week cycle. In addition, ACNU (2-3 mg/kg) was given on the 2nd day of each cycle. Conventional focal irradiation (1.5-2 Gy/day for 5 days to a total dosage of 40-60 Gy) was administered beginning on day 3. Patients underwent at least two 6-week cycles. Adverse effects included nausea, vomiting, and myelosuppression, but were mild and transient. Response to treatment was evaluated by the reduction in tumor size measured on postcontrast computed tomographic scans and magnetic resonance images. Responses occurred in 10 of 11 patients with the intrinsic type of brainstem glioma, including three complete and seven partial responses. Two of five patients with exophytic type gliomas partially responded. The median survival was 15.7 months, a remarkable improvement over the natural course of this disease. These results indicate that IAR therapy is a useful primary treatment for pediatric patients with brainstem gliomas.
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PMID:Effectiveness of interferon-beta, ACNU, and radiation therapy in pediatric patients with brainstem glioma. 128 18

A region of chromosome 9, surrounding the interferon-beta (IFNB1) locus and the interferon-alpha (IFNA) gene cluster on 9p13-p22, has been shown to be frequently deleted or rearranged in a number of human cancers, including leukemia, glioma, non-small-cell lung carcinoma, and melanoma. To assist in better defining the precise region(s) of 9p implicated in each of these malignancies, a combined genetic and physical map of this region was generated using the available 9p markers IFNB1, IFNA, D9S3, and D9S19, along with a newly described locus, D9S126. The relative order and distances between these loci were determined by multipoint linkage analysis of CEPH (Centre d'Etude du Polymorphisme Humain) pedigree DNAs, pulsed-field gel electrophoresis, and fluorescence in situ hybridization. All three mapping approaches gave concordant results and, in the case of multipoint linkage analysis, the following gene order was supported for these and other closely linked chromosome 9 markers present in the CEPH database: pter-D9S33-IFNB1/IFNA-D9S126-D9S3-D9S19 -D9S9/D9S15-ASSP3-qter. This map serves to extend preexisting chromosome 9 maps (which focus primarily on 9q) and also reassigns D9S3 and D9S19 to more proximal locations on 9p.
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PMID:Genetic and physical map of the interferon region on chromosome 9p. 138 97

The possibility for new interferon therapy was investigated using the effect of endogenous human interferon-beta (HuIFN-beta) on various culture cell lines. Cell lines were exposed to superinduction agents (poly I: poly C, cycloheximide, and actinomycin D) and the production of endogenous interferon analyzed. Quantitative determination of HuIFN-beta and messenger ribonucleic acid (mRNA) showed HuIFN-beta was induced in all of five glioma cell lines, one of two melanoma cell lines, and all of three lung carcinoma cell lines as well as fibroblasts. Northern blot analysis showed HuIFN-beta mRNA induced in glioma cells was identical to that from fibroblasts. Endogenous HuIFN-beta induced from glioma cells had a cytostatic or cytocidal effect against various human glioma cell lines, even those resistant to fibroblast-derived HuIFN-beta. These results show it may be possible to use the induction of excess endogenous cytotoxic HuIFN-beta in human glioma tissue itself.
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PMID:Superinduction of cytotoxic interferon-beta in glioma cells. 172 75

The distribution of 125I-labelled recombinant mouse interferon-beta (rMuIFN-beta) in normal and glioma (203 glioma) bearing mice was studied by radioassay and macro-autoradiography at 15 and 30 min after a single intravenous injection. The level of rMuIFN-beta in the spleen was about 20-fold higher than in serum. Concentrations higher than the serum level was detected in the lung, liver and kidney. The concentration of rMuIFN-beta in the brain was 8% of the serum level and the concentration in the glioma 30 min after administration was about 10-fold higher than in normal mouse brain. Macro-autoradiographic study demonstrated a wide distribution range and selective uptake in glioma tissue. Furthermore, we found that mouse gliomas were sensitive to mouse IFN-beta. Our findings demonstrate that in the mouse glioma model, intravenously administered interferon reaches the tumour.
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PMID:Distribution of mouse interferon-beta in normal and brain tumour-bearing mice. 206 66

The antiproliferative effects of human recombinant interferon-alpha (rIFN-alpha A) and interferon-beta (rIFN-beta ser) were assessed in vitro against seven human glioma cell lines. Further analysis of one of these lines (EFC-2) in response to rIFN-alpha A demonstrated a minimum growth inhibition by day 6 of treatment, whereas a 50% inhibition of cell growth was observed with a dose of 50 U/ml of IFN-beta ser. No significant growth inhibition was seen by rIFN-alpha A at doses up to 500 U/ml. Addition of rIFN-alpha A to rIFN-beta ser-treated EFC-2 cells neither suppressed nor augmented the antiproliferative response to IFN-beta ser. The binding of 125I-labeled rIFN-alpha A or 125I-labeled rIFN-beta ser to EFC-2 cells was inhibited competitively by increasing concentrations of either unlabeled rIFN-alpha A or rIFN-beta ser. This suggests that the cellular receptors for both rIFN-alpha A and rIFN-beta ser appear to be intact and appear to bind both agents equally. Furthermore, incubation of EFC-2 cells for 72 h with either rIFN-alpha A or rIFN-beta ser resulted in an increase in 2',5'-oligoadenylate (2-5A) synthetase activity 5-fold with rIFN-alpha A and 50-fold with rIFN-beta ser. Similarly, the 68-kD IFN-induced protein kinase was induced substantially with rIFN-beta ser but only slightly induced with rIFN-alpha A treatment. These results suggest that EFC-2 human glioma cells demonstrate a differential sensitivity in terms of growth inhibition to rIFN-beta ser and to rIFN-alpha A which appears to correlate with a differential induction of both intracellular 2-5A synthetase and protein kinase activity. These results cannot be explained solely on the basis of surface receptor binding of rIFN-alpha A and rIFN-beta ser. These data do suggest that, for human glioma cells in culture, type I IFN receptors may display a subtle architectural variation that allows equivalent binding of both IFN-alpha and IFN-beta ser, but allows an enhanced signal transduction and biological effect only after binding a specific IFN subtype.
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PMID:Growth inhibitory effects of interferon-beta but not interferon-alpha on human glioma cells: correlation of receptor binding, 2',5'-oligoadenylate synthetase and protein kinase activity. 214 Mar 95

The efficacy of radiation.MCNU (MR group) or radiation.MCNU.interferon-beta (IMR group) for malignant glioma was studied by a randomized trial at numerous medical facilities. MR group was irradiated with 50-60 Gy and intravenously injected with 2 mg/kg of MCNU on the initial day of irradiation and 6 weeks later. IMR group was also given intravenous administration of interferon-beta at the dose of 2 x 10(6) IU/m2 for 5 serial-days every eight weeks. There was no difference in background between the two groups. The response rate in MR group and IMR group was 44.4% (4/9) and 30.0% (3/10), respectively, showing no significant difference. The resected tumor volume before the start of these regimens seemed to correlate the response to the treatment in both groups. The major toxicity was myelosuppression, especially using MCNU with interferon-beta. These results indicated that this combined therapy is effective for malignant glioma, and should be executed further trials and follow up study.
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PMID:[Randomized study of initial treatment with radiation.MCNU or radiation.MCNU.interferon-beta for malignant glioma. Hiroshima Brain Tumor Study Group]. 240 77

Antiproliferative activity of recombinant murine interferon-beta (Rec-MuIFN-beta) combined with hyperthermia against Rous sarcoma virus-induced mouse malignant glioma (RSV glioma) was investigated both in vitro and in vivo. In vitro, the antiproliferative activity of Rec-MuIFN-beta was enhanced by incubation at elevated temperatures (40 degrees and 43 degrees C). In vivo, combined therapy of Rec-MuIFN-beta treatment and local tumour hyperthermia (43 degrees C) exerted a greater antitumour effect against transplanted RSV glioma in C3H/He mice than either treatment alone, especially when Rec-MuIFN-beta was administered intratumourally. Subsequently, in order to probe the mechanism of enhanced antiproliferative activity, the production of prostaglandin E2 (PGE2) and 2', 5'-oligoadenylate synthetase (2-5A synthetase) in the culture medium of RSV glioma cells was measured. Rec-MuIFN-beta treatment resulted in a significantly greater PGE2 and 2-5A synthetase production at 43 degrees C than at 37 degrees C.
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PMID:Antitumour effect of interferon combined with hyperthermia against experimental brain tumour. 348 Mar 23

A study was made on the antitumor effect of recombinant murine interferon-beta (rMuIFN-beta) against virus-induced mouse malignant glioma. In in vitro experiments, a dose-dependent and a time-dependent manner were observed for 24 h in the antiproliferative activity of rMuIFN-beta. In in vitro experiments, the growth of subcutaneously transplanted gliomas in mice treated with intraperitoneal administration of rMuIFN-beta was inhibited slightly, whereas, with intratumoral administration, it was inhibited more effectively. In immunological studies, natural killer (NK) cell and cytotoxic T-lymphocyte activities of spleen cells were enhanced with intraperitoneal administration of rMuIFN-beta. The analysis of IFN-induced change in a subpopulation of peripheral blood lymphocytes revealed a decrease of Thy.1,2-positive cells and an increase in the ratio of Lyt.1/Lyt.2-positive cells. But these immunological effects of rMuIFN-beta declined on the 7th day with daily administration. Such hyporeactivity may be noteworthy for the clinical application of IFN.
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PMID:Antitumor effect of recombinant murine interferon-beta against mouse malignant glioma. 349 13

The antitumor efficacy of recombinant interferon-beta (rIFN-beta) on human glioblastomas was investigated in vitro and in meningeal gliomatosis(MG) models. A total of 1.5 X 10(5) human glioma (ONS-12 and ONS-20) cells were suspended in 2 ml of RPMI-1640 with 10% fetal calf serum and placed in plastic dishes (Falcon #3001). rIFN-beta 10(2)-10(5) units were then added to each culture dish on days 3, 5 and 7. Both ONS-12 and ONS-20 human glioma cells were suppressed with a low dose of rIFN-beta. As MG models, 5 X 10(7) ONS-12 glioma cells were suspended in saline and transcutaneously inoculated into the cisterna magna of BALB/c nu/nu mice using a 27-gauge needle. The median survival times (MST) of MG models which were treated by intrathecal administration of 10(3) U of rIFN-beta and intraperitoneal injection of 10(4) U of rIFN-beta were 11.0 and 8.0 days, compared with an MST of 7 days for control mice. The rIFN-beta was not effective by intraperitoneal administration but was effective by intrathecal administration in the MG models. The MSTs of MG models which were treated by administration of 10(5) U, 10(3) U of rIFN-beta and 0.1 ml saline were 15.0, 19.0 and 9.0 days, respectively. The therapeutic efficacy in MG models depended on the administration route of rIFN-beta, and as far as could be determined from the MG models, high-dose administration of rIFN-beta was not always useful.
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PMID:[Antitumor efficacy of recombinant interferon-beta on human glioma]. 381 77

The purpose of this investigation is to elucidate antitumor activity of human interferon-beta (Hu IFN-beta) against nervous system tumors. The study of growth inhibition in vitro with IFN against a variety of human glioma and neuroblastoma cell lines showed a significant response with sensitive cell lines at the concentration of 1 X 10(3) IU/ml in the medium. With resistant cell lines, however, tumor cells were proliferated as control even at the concentration of 10(4) IU/ml. The activation of lymphocyte-mediated cytotoxicity was also studied. The microcytotoxicity test with AJ glioma cells as target was used to evaluate it. In this system, percentage of cytotoxicity was 33 +/- 10.0% by lymphocytes obtained from six healthy adult men and four patients with malignant glioma, and it was increased to 71 and 72% seven days after intravenous administration of IFN (daily dose 3 X 10(6) IU) for the treatment of gliomas. The results indicate that human IFN-beta is considered effective in the treatment of malignant gliomas.
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PMID:[Effect of interferon on malignant brain tumor]. 718 55


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