Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017636 (glioblastoma)
 18,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A defective subacute sclerosing panencephalitis (SSPE) virus which had been passaged in human embryonic lung cells was transferred to cultures of three neural cell types: neuroblastoma, oligodendroglioma and glioblastoma. The growth characteristics of the virus in these cells were essentially similar to those in non-neural cells. On the other hand, a marked difference in neurovirulence was noticed for the virus grown in neural cells when examined by intracerebral inoculation into mice. The virus passaged in neuroblastoma and oligodendroglioma cells showed high neurovirulence, inducing an acute encephalitis, whereas the virus passaged in human embryonic lung cells and that in glioblastoma cells did not show neurovirulence. These results suggest that the virus recovered its neurovirulence after passage in certain human neural cells.
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PMID:Growth of defective subacute sclerosing panencephalitis viruses in human neural cells and their neurovirulence in mice. 298 73

This article reviews current morbidity and mortality statistics for the major classes of primary brain tumors including malignant astrocytoma, glioblastoma, low-grade astrocytoma, oligodendroglioma, meningioma, and other benign tumors and metastatic tumors. Innovations in therapy are discussed for surgery, radiation, chemotherapy, and such newer areas as hyperthermia, immunotherapy, and phototherapy.
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PMID:The morbidity and mortality of brain tumors. A perspective on recent advances in therapy. 299 25

The purpose of this study is to present the methodology and results of a clinical trial of local chemotherapy of malignant brain tumors based on slowly-releasing anticancer drug-polymer composites. The slowly releasing drugs were prepared by combining and mutually dispersing anticancer agents with glassified monomers containing 10% polymetacrylic methyl acid and then this compound was frozen at -78 degrees C and exposed to 1 X 10(6) rad of gamma rays from cobalt 60. Thus we prepared a compound of polymers and anticancer agents. We used needle-shaped capsules of this compound. These capsules release the drug very slowly over 40 days. We administered locally to the malignant brain tumors with either slowly releasing mitomycin, slowly releasing adriamycin, slowly releasing ACNU or slowly releasing 5 Fu drugs. The following techniques were employed in implantation these capsules. Implantation into the remaining tumor wall at the time of excision. Implantation into the tumor by CT-guided stereotactic method. We implanted these drugs into tumor of 55 cases, thereafter we conducted both radiation and chemotherapy with ACNU in most patients. This method has the following advantages: It is possible to be employed to different types of anticancer agents. Both dosage and releasing time can be adjusted. It is possible to administer these capsules postoperatively by the stereotactic method. The clinical study consists of 55 patients, 20 cases of anaplastic astrocytoma, 23 cases of glioblastoma multiforme, 5 cases of oligodendroglioma, 3 cases of medulloblastoma and 4 cases of others. Survival rate estimated by Kaplan-Meier method was 47% in glioblastoma at 12 months and 91% in anaplastic astrocytoma at 18 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of malignant brain tumors with slowly releasing anticancer drug-polymer composites]. 302 49

The immunoblotting technique was used to study the glycoproteins in human brain tumor samples including astrocytoma, glioblastoma, meningioma and oligodendroglioma, as well as in normal human brain. Glycoproteins were separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis, electrophoretically transferred to nitrocellulose membrane and characterized, using binding with 11 different lectins. Tumor-associated glycoproteins were found using the lectins peanut agglutinin (PNA), soybean agglutinin, Limulus polyhemus, Lotus tetragonolobus, Ricinus communis 1, (RCA-1) and wheat germ agglutinin (WGA). Their molecular masses ranged from 50 to 180 kDa. Several of them were common to the 3 types of tumors: astrocytomas, oligodendrogliomas and meningiomas. PNA, RCA-1 and WGA were the 3 most feasible lectins with regard to tumor specificity, simplicity and reproducibility.
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PMID:Glycoprotein pattern in human brain tumors studied using lectin binding after sodium dodecyl sulfate-gel electrophoresis and protein blotting. 303 65

Type beta transforming growth factor (beta-TGF) is a potent regulator of cell growth and differentiation. The human glioblastoma cell line, T-MGI, was growth inhibited by beta-TGF under anchorage independent conditions. The antiproliferative effect of beta-TGF was potentiated to nearly total arrest by low doses of retinoic acid (RA) or tumor necrosis factor (TNF), while epidermal growth factor, platelet-derived growth factor, interleukin-2, and gamma interferon did not have this potentiating effect. The potentiation of the beta-TGF effect by RA and TNF could not be explained by modulation of the epidermal growth factor receptor, the beta-TGF receptor, or the TNF receptor. beta-TGF alone and in combination with RA or TNF were further tested on primary cultures from freshly resected human glioma biopsies (n = 13). There was great individual variation in sensitivity to beta-TGF, RA, or TNF. The astrocytoma and oligodendroglioma cells were inhibited to various degrees by beta-TGF or TNF, while most of the glioblastomas were not sensitive to these agents. Most of the biopsies were stimulated by RA. RA or TNF did not potentiate the growth inhibitory effect of beta-TGF on biopsy cells. We therefore think it unlikely that beta-TGF in combination with RA or TNF will be effective agents in the treatment of gliomas.
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PMID:Effects of type beta transforming growth factor in combination with retinoic acid or tumor necrosis factor on proliferation of a human glioblastoma cell line and clonogenic cells from freshly resected human brain tumors. 316 58

This study was undertaken to determine the maximum tolerated dose of aziridinylbenzoquinone (AZQ) given as a 24-hour intravenous infusion every 21-28 days. Thirty-four patients with recurrent or progressive gliomas received AZQ at a dose of 25, 30, 35, 40, or 45 mg/m2. At a dose of 45 mg/m2, leukopenia and thrombocytopenia of grade 3 or greater was observed in 42% and 25% of patients respectively; no patient required transfusion or antibiotics for fever. For administration of AZQ at a 24-hour intravenous infusion, we recommend a starting dose of 40 mg/m2 for patients without previous exposure to cytotoxic agents, and 35 mg/m2 for patients treated with such agents. In 14 patients with glioblastoma, tumor regression was observed in 1 patient (14%) and stabilization of disease was demonstrated in 7 patients (50%). In 17 patients with anaplastic astrocytomas there were no responses, but 8 patients (47%) stabilized. Of two patients with an oligodendroglioma, one continues without progression at 34 weeks after initial response. One patient with malignant ependymoma stabilized and had not progressed at 39 weeks. The median time to tumor progression in patients who stabilized and responded was 18 weeks for those with glioblastoma multiforme and 16 weeks in those with anaplastic astrocytomas.
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PMID:A phase I/II study of 24 hour intravenous AZQ in recurrent primary brain tumors. 322 Dec 59

The biochemical characteristics of canine distemper virus (CDV) adapted to three human neural cells (glioblastoma, oligodendroglioma, and neuroblastoma cells) were compared with those of the unadapted original virus. The specific gravity of the virions and nucleocapsids of the original and the three adapted viruses were not different. The molecular weights of genomic RNA and messenger RNAs encoding H, F, P, and NP proteins of the adapted viruses as estimated by Northern blot hybridization were similar to those of the original virus. By T1-resistant oligonucleotide analysis of the genomic RNA, the glioblastoma- and the neuroblastoma-adapted viruses gave two more spots than the original virus; the oligodendroglioma-adapted virus had a pattern identical to that of the original virus. By two-dimensional gel electrophoresis of virion proteins, we found a difference in the isoelectric point of the viral envelope proteins H and F between the original and the adapted viruses. These results suggest that viral genomic changes occurred during adaptation, resulting in the alteration of viral envelope proteins.
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PMID:Characterization of canine distemper viruses adapted to human neural cells. 323 21

The stability of neurovirulence and in vitro phenotypes of canine distemper viruses adapted to neural cells was examined. Neurovirulence was estimated by the morbidity, mortality, and histopathological changes in the central nervous system of mice. After a single passage of the adapted viruses in Vero cells in which the unadapted virus had been passed, the neurovirulence of glioblastoma-adapted and oligodendroglioma-adapted viruses reverted completely to that of the unadapted virus. However, the neurovirulence of a neuroblastoma-adapted virus reverted partially. In vitro phenotypes such as the two-dimensional electrophoretic patterns of viral proteins and the cross-neutralization patterns also reverted to those of the unadapted virus. However, plaque sizes remained similar to those of the viruses adapted to neural cells.
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PMID:Reversion of neurovirulence and in vitro phenotype of neural cell-adapted canine distemper virus after passage in non-neural cells. 323 24

This report presents a flow-cytometric analysis of cellular DNA in biopsies and primary cell cultures of 21 human astrocytomas and 19 oligodendrogliomas. A distinct correlation between histological dedifferentiation and pathological DNA distribution was found. Classification was made according to increasing histological anaplasia, corresponding to a four-grade scale and proliferation index (PI). Four types of gliomas were defined according to characteristic DNA patterns and proliferative activities in comparison to their histological grading: 1. purely diploid DNA patterns with low 4C (premitotic) peaks and PI values up to 10 in well-differentiated gliomas; 2. increase of tetraploid cells and PI of 10-16 in tumors with histological grades II or II-III; 3. diploid-tetraploid DNA distribution with PI values up to 30-31 and malignancy grade III; 4. polyploid and aneuploid karyograms with excessive 4C increase, emerging in grade III and especially grade III-IV of these gliomas. Varying DNA distribution during tumor development could be observed in a malignant transformation of an oligodendroglioma I to a glioblastoma after a course of 3 1/2 years. A more detailed subdivision of these tumors according to their DNA content and proliferative activity was achieved. With the exception of occasional variation in karyograms, DNA distribution usually remained stable in primary tissue cultures (PTC).
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PMID:Flow cytometric analysis of cellular DNA content in human astrocytomas and oligodendrogliomas. 324 16

Neurovirulence of the Onderstepoort strain of canine distemper virus (CDV) adapted to human neural cell lines was determined by the intracerebral inoculation of DDD mice at 3 and 5 weeks of age. Intensity of neurovirulence was estimated by histopathological changes in the central nervous system and clinical symptoms. The original virus propagated in Vero cells induced leptomeningoencephalitis, whereas neuroblastoma-adapted virus induced nerve cell degeneration and mild encephalitis with relatively low morbidity and fatality. In contrast, the viruses adapted to glioblastoma and oligodendroglioma caused high morbidity and fatality. The latter two viruses induced necrotizing encephalopathy including edema and hyperemia. In addition, the glioblastoma-adapted virus induced formation of giant cells. The oligodendroglioma-adapted virus caused demyelination and spongy state associated with degeneration of glial cells and axons. These observations are discussed in regard to a possible correlation between the neurovirulence of CDV in mice and its tropism for neural cells in vitro.
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PMID:Neurovirulence in mice of neural cell-adapted canine distemper virus. 372 59


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