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)

Recently, it has been reported that CDDP modifies the immune responses of tumor bearing hosts, but problem of the most appropriate treatment with CDDP to augment the host immunity remains unresolved. The purpose of this study was to determine the most advantageous administration of CDDP to increase both its cytotoxic effect and antitumor immune reactivity. Cell growth inhibition in vitro was assessed by MTT assay after treatment of U-251MG cells with various concentrations of CDDP for 24 or 120 hours. The results of this experiment showed that the growth of U-251MG cells in vitro was suppressed by CDDP in a dose-dependent as well as a time-dependent manner. Ten days after subcutaneous inoculation of human glioma cells, GL-9, in the rear flank of nude mice, they were assessed for growth suppression by CDDP. Totally, 20 ml/kg of CDDP was administered to each mouse; in one group (high-dose CDDP group), 5 ml/kg of CDDP on every fifth day, and in the other group (low-dose CDDP group), 2 ml/kg on every day. Measurement of the tumor volume in each group revealed no significant difference between the two groups in terms of the efficacy of tumor growth suppression. Twenty-one days after inoculation, we measured the splenic natural killer(NK) cell activity in each mouse. The results showed that NK cell activity was significantly increased in the low-dose cisplatin (2 ml/kg) group, and significantly decreased in the high-dose cisplatin (10 mg/ml) group, as compared to the control group. The results of our study suggest that the separate administration of low-dose CDDP is a useful treatment strategy for malignant glioma, because it increases the antitumor immune reactivity of hosts without decreasing the direct tumor cytotoxicity of CDDP.
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PMID:[Effects of separate administration of low-dose CDDP on antitumor immune reactivity for treatment of malignant glioma]. 766 72

Specific and recurring chromosomal and genetic alterations have been identified in gliomas and could described a model of tumoral progression from benin glioma to glioblastoma multiforme. However, the heterogeneity of profiles of molecular alterations that have been observed in gliomas seems to reflect the variety of clinical evolutions which characterise those tumors. Loss of genetic material on chromosomes 17, 9 and 19, then of chromosome 10 have been associated to pathogenesis of glioma and a pejorative prognostic value have been attributed to the alteration of chromosome 10. Gliomas also express growth factors and growth factors receptors that may be important in promoting tumor growth, like Epidermal growth factor (EGF), fibroblast growth factors (FGF) and vascular endothelial growth factor (VEGF). Tumoral invasion which characterise also gliomas, may involve proteases like plasminogen activators (PA) and metalloproteases, under the regulation of specific receptors and inhibitors. PA inhibitor type 1 (PAI1), associated to the most aggressive form of gliomas, may also participate to tumoral neoangiogenesis. Description and understanding of these alterations may contribute to develop new treatment modalities in gliomas.
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PMID:[Biological profiles of malignant gliomas]. 767 50

The effect of human recombinant interleukin-1 beta (hrIL-1 beta) on tumor growth was studied in eight glioma cell lines. hrIL-1 beta inhibited growth in all cell lines, but to varying extents. Two cell lines were suppressed by 0.5 ng/ml hrIL-1 beta, and three cell lines required 20 ng/ml. hrIL-1 beta also induced morphological changes and increased F-actin contents. hrIL-1 beta-treated cells demonstrated multipolar shapes and numerous processes with a greater number of cell-cell contacts 24 hours after treatment. Fluorescence microscopy revealed that these processes contained a large amount of polymerized F-actin. These results suggest that hrIL-1 beta-mediated growth inhibition may be related to the differentiation of glioma cells.
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PMID:Human recombinant interleukin-1 beta-mediated growth inhibition of cultured malignant glioma cells. 768 Jul 76

Angiogenesis, a process dependent upon perivascular proteolysis, is required for solid tumor growth and is inhibited by certain steroids including glucocorticoids. We examined the relationship between tumor growth and vessel density in experimental rat brain 9L glial tumors following chronic treatment with the glucocorticoid dexamethasone. Tumor growth was inhibited by intraperitoneal administration of 3 mg/kg/day dexamethasone. Maximal cross-sectional areas of post-implantation day 9 tumors were 4.6 +/- 1.0 mm2 in dexamethasone-treated animals and 17.0 +/- 3.4 mm2 in controls (P < 0.01). Microvessel density assessed by laminin immunohistochemistry was 59% lower in dexamethasone-treated tumors (P < 0.01). Plasminogen activator (PA) activity, a proteolytic enzyme related to endothelial migration and vessel growth, was 4.2 +/- 0.9 IU/micrograms protein in dexamethasone-treated tumors and 9.0 +/- 1.0 IU/micrograms protein in control tumors (P < 0.01). Exposure of cultured 9L and central nervous system microvessel endothelial cells to dexamethasone concentrations comparable to those achieved in vivo had no effect on cell growth, but reduced the PA activity of culture supernatant fractions by 78% and 99%, respectively. These findings suggest that inhibition of proteolytic steps involved in vessel growth may underlie, in part, the mechanism by which glucocorticoids decrease brain tumor growth.
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PMID:Dexamethasone reduces vascular density and plasminogen activator activity in 9L rat brain tumors. 768 48

The morphology of supratentorial malignant glioma was examined in autopsy brains from three anaplastic astrocytoma and 11 glioblastoma multiforme patients. Large histological preparations and routine preparations were used to investigate the primary lesion site, infiltration to adjacent brain, and cerebrospinal fluid (CSF) dissemination. The primary lesion sites showed active tumor growth with mass effect in three cases, necrotic tumor and brain with no or mild mass effect in nine, and no residual tumor in two. Tumor infiltration included extensive bilateral cerebral hemisphere infiltration in seven cases, moderate infiltration of one or two lobes in three, minimal infiltration just beyond the tumor bed in two, and no infiltration in two. Infiltration occurred along the fiber tract and subependymal tissue. CSF tumor cell dissemination occurred in the ventricular system in two cases, cerebral subarachnoid space in five, and spinal subarachnoid space in one. Small fibrillated cells and small anaplastic cells predominated in infiltrated lesions and CSF dissemination.
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PMID:Pathological anatomy of autopsy brain with malignant glioma. 768 69

Interferons (IFNs) are a natural body defense with powerful effects on tumor growth, including gliomas. The direct effects of IFN-gamma on (1-4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU)-induced deoxyribonucleic acid (DNA) damage and cytotoxicity were investigated in two human glioblastoma cell lines, A-172 and T98G, using a single cell microgel electrophoresis technique and a microculture tetrazolium assay. The results demonstrated a synergistic effect of IFN-gamma with ACNU on intracellular damage in both cell lines. 10 micrograms/ml ACNU induced a cell inhibition rate of 23.9% in A-172 cells, and almost no effect on T98G cells. 1000 U/ml IFN-gamma and 10 micrograms/ml ACNU caused a significant increase in cell inhibition, 51.2% for A-172 and 72.3% for T98G cells. DNA damage in individual A-172 and T98G cells exposed to ACNU was enhanced significantly by IFN-gamma (p < 0.001). The findings suggest a direct effect of IFN-gamma on ACNU-induced cell damage in human glioma, in addition to its effect on immunomodulation.
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PMID:Effect of interferon-gamma on ACNU-induced DNA damage and cytotoxicity in human glioblastoma cells. 768 31

Two aspects of cytokine therapy of intracerebral tumors are considered in this study: modulation of tumor growth in vivo and central nervous system toxicity. Coimplantation of RG-2 glioma cells and retroviral vector producer cell lines was performed to provide a local source of interleukin-2 (IL-2) or IFN-gamma within the tumor and coinitiate an antitumor immune response. We demonstrated that local intratumoral production of IL-2 and IFN-gamma generates a cell-mediated antitumor response in vivo. This response was manifest as a diffuse infiltration of monocytes/macrophages, CD4+ and CD8+ T cells, and activation of microglial OX42+ cells in intracerebral RG2 tumors. The cell-mediated antitumor immune response resulted in the early suppression of intracranial and subcutaneous tumor growth, but the effect was not sustained and there were no tumor regressions. The absence of increased survival of animals with intracranial tumors is explained in part by the severe central nervous system toxicity caused by local production of IL-2 and IFN-gamma. Central nervous system toxicity induced blood-brain barrier disruption, vasogenic brain edema, and dislocation of the brain midline structures, as observed by dynamic magnetic resonance imaging and direct measurements of tissue water content. The clinical application of IL-2 and IFN-gamma gene transfer therapy for intracerebral tumors must consider the potential for severe vasogenic brain edema associated with intracerebral production of these cytokines.
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PMID:RG-2 glioma growth attenuation and severe brain edema caused by local production of interleukin-2 and interferon-gamma. 772 57

Optic pathway gliomas (OPG) are found in about 15% of patients with neurofibromatosis Type 1 (NF-1). The natural history of OPG is not yet well documented. Treatment in cases with growing tumors is still controversial. Twenty-one patients with NF-1 and OPG, diagnosed over a 20-year period, and followed neuroradiologically and ophthalmologically for at least two years, were reevaluated. The diagnosis of OPG was made at a mean age of 7.1 years (range 0-14.5 years); six children were asymptomatic, 15 were symptomatic. The mean follow-up was 9.0 years (2.0-18.5 (years). In eight initially operated or biopsied patients (three optic nerve and five chiasmal gliomas) tumor regrowth was found in one patient without progression on subsequent follow-up. Improvement of visual acuity occurred in one child after operation of a large suprasellar tumor and deterioration in one patient after biopsy of a chiasmal glioma. The neuroradiological follow-up of the 13 not-operated and not-radiated patients (four optic nerve and nine chiasmal gliomas) was stable in 10, progressive in three, resulting in visual loss in one patient. In 11 children (52%) a second tumor outside the optic pathway was found at a mean age of 4.0 years after the diagnosis of an OPG. Until now they are mostly asymptomatic. Second site tumors were operated in two children because of rapid tumor growth, one child died of a brainstem tumor. OPG are a frequent complication in children with NF-1, appearing within the first decade.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Follow-up of optic pathway gliomas in children with neurofibromatosis type 1. 777 Jan 26

In our previous study on liposome-mediated transfection of the human interferon-beta (HuIFN-beta) gene into subcutaneously implanted human gliomas in nude mice, we found that HuIFN-beta was produced and secreted by the tumor cells and that the growth of solid tumors was completely inhibited. The present study investigated the growth-inhibitory effect of liposomes containing the HuIFN-beta gene inserted into a vector (pSV2IFN-beta) on T9 rat glioma implanted into the brains of rats. Tumor cells and liposomes containing pSV2IFN-beta or other additives were simultaneously injected into the brains of rats. HuIFN-beta was detected in solid gliomas growing in the brains of rats injected with liposomes and magnetic resonance imaging (MRI) showed that tumor growth was inhibited. In addition, the latent period until the appearance of neurological symptoms was significantly prolonged in rats treated with liposomes containing pSV2IFN-beta. However, the survival time of the treated rats was not significantly increased.
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PMID:Growth inhibition of intracerebral rat glioma by transfection-induced human interferon-beta. 777 50

The purpose of this study was to evaluate the anti-tumor activity of sequenced administration of O6-benzylguanine (BG), streptozotocin (STZ), and 1,3-bis(2-chloroethyl)-1- nitrosourea (BCNU) in vitro and in vivo. We measured the recovery of O6-methylguanine DNA methyltransferase (MGMT) and BCNU cytotoxicity in the human glioma SF767 cell line, and anti-tumor activity against xenografts following exposure to BG, STZ or the combination of BG + STZ combined with BCNU. In SF767 cells, the combination of BG (10 microM) + STZ (0.05 mM) produced sustained inhibition of MGMT activity for at least 24 hr, and a greater potentiation of BCNU cytotoxicity than either agent alone. The combined treatment of BG + STZ increased BCNU-induced cell kill by 0.5 to 1.0 log over BG or STZ alone. The maximally tolerated doses of the combination of BG + STZ + BCNU administered to nude mice i.p. were the following: BG (80 mg/kg), STZ (100 mg/kg), and BCNU (15 mg/kg). Utilizing these doses of BG and STZ, the depletion and repletion profile of MGMT activity in SF767 xenografts was measured. STZ at 100 mg/kg did not affect xenograft MGMT activity. Subsequent to BG treatment, xenograft MGMT activity was inactivated completely for 12 hr, and the tumors gradually recovered approximately 40% of control activity by 24 hr. The combination of BG + STZ produced sustained inhibition of MGMT activity for 24 hr in the xenografts with complete recovery of MGMT activity by 48 hr. Administration of the combination of BG + BCNU to nude mice bearing SF767 tumor resulted in significant inhibition of tumor growth for 23 days. However, the addition of STZ to this combination provided no greater anti-tumor activity than that observed with BG + BCNU. The three-drug combination of BG, STZ, and BCNU produced no more than 2.4 to 13.0% weight loss with occasional lethal toxicity. Collectively, these data suggest that prolonged depletion of MGMT might be required for optimal reversal of BCNU resistance both in vitro and in vivo.
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PMID:Anti-neoplastic activity of sequenced administration of O6-benzylguanine, streptozotocin, and 1,3-bis(2-chloroethyl)-1-nitrosourea in vitro and in vivo. 780 3


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