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)

Alpha and beta interferon were tested for antitumor activity and clinical toxicity in 15 children suffering from cancer. The drug was administered IV, IM, IT or intralesionally daily in the majority of cases in total doses of 18 X 10(6) to 9,634 X 10(5) IU. Major toxicities were a flulike syndrome, elevation of transaminase activity and leukopenia. A minor response (less than 50%) was observed in one patient with glioblastoma, treated by intrathecal administration, and an objective local response was noted in one rhabdomyosarcoma patient with multiple subcutaneous metastases, who was treated by intralesional administration. CNS leukemia in two patients improved without hematological response. Further trials are warranted.
Gan To Kagaku Ryoho 1984 Sep
PMID:[Clinical experience with alpha and beta interferon in childhood cancer]. 659 60

Since 1980, phase 1 and 2 clinical trials of Hu-IFN-beta have been done in the field of neurosurgery. In the present study, (1) the results of in vivo experiments of Hu-IFN-beta are reported and (2) the effectiveness of Hu-IFN-beta in patients with malignant brain tumors is also evaluated. (1) The antitumor activities of beta-IFN and poly ICLC in nude mice receiving subcutaneous transplants of human brain tumors (2 strains) were compared with those of conventional anticancer drugs. After 3 weeks of treatment with ACNU, vincristine, bleomycin, mitomycin C, beta-IFN and poly ICLC, tumor reduction rates were evaluated by the method of Battelle. The effectiveness of beta-IFN and poly ICLC was slightly inferior to that of ACNU and vincristine, although tumor reduction rates (treated/control values) of 43% and 39% were respectively obtained with beta-IFN and poly ICLC against one strain of glioblastoma. (2) Clinically, 7 patients with malignant brain tumors were given beta-IFN (4 by intratumor administration and 3 by intravenous injection) in a dose of 3 X 10(6) to 9 X 10(6) IU/day for 2 to 6 months to study the efficiency and side effects of IFN treatment. One of four patients given IFN intratumorally showed a reduction in tumor size (partial response) by CT scan; the three patients injected IFN intravenously were unchanged. There were no noteworthy side effects in the cases treated intratumorally except for fever occurring in one patient. In the patients treated intravenously, however, fever, general malaise, leukopenia and thrombocytopenia were noted.
No To Shinkei 1983 Sep
PMID:[Effect of human fibroblast interferon on malignant brain tumors]. 665 89

We investigated the effects of local administration of interferon (IFN) on 13 patients with recurrent brain tumors. Histologic diagnoses were glioblastoma (eight patients), medulloblastoma (one), ependymoma (one), ependymoblastoma (one), pontine glioma (one), and astrocytoma (one). When tumor recurrence was evident local administration of IFN was started through an Ommaya reservoir, which was placed during repeat craniotomy. No tumor regressions were seen in the patients given weekly injections of IFN; however, in two of six patients given daily injections, a decrease of tumor volume and augmentation of natural killer activity were seen.
Cancer Treat Rep 1983 Sep
PMID:Local administration of interferon for malignant brain tumors. 668 76

Ventriculoperitoneal shunting has been accepted as a safe and useful preliminary procedure that lowers the mortality and morbidity of definitive surgery for tumors causing obstructive hydrocephalus. We are reporting four patients with intratumoral hemorrhage as a complication of shunting. The hemorrhage was massive and fatal in two patients, one with an unverified pineal tumor and the other with a malignant astrocytoma of the thalamus. The hemorrhage was small and limited in the other two patients, one with a glioblastoma of the thalamus and the other with a cerebellar astrocytoma. On the basis of this experience, we conclude that the possibility of intratumoral hemorrhage should be taken into consideration when planning the preoperative management of obstructive hydrocephalus caused by brain tumors. It is possible that ventricular decompression may result in rapid motion and distortion of the intracranial structures and a sudden imbalance between intracranial and intratumoral pressures, leading to vascular insufficiency, congestion, and then hemorrhage within the tumor.
Neurosurgery 1981 Sep
PMID:Intratumoral hemorrhage after a ventriculoperitoneal shunting procedure. 730 Oct 65

A New cell line, U-706, established from an uncommon human glioma (possibly giant-cell glioblastoma) is reported in this communication. The tumor gave rise to two permanent sublines, one attached (U-706M) and one non-attached (U-706S) cell line. The growth characteristics, chromosome banding pattern, electronmicroscopic picture and cell surface characteristics of the two sublines are described.
Int J Cancer 1981 Sep 15
PMID:Establishment of attached and non-attached cell lines from an uncommon human glioma. 731 77

In this study, a differential display method for messenger ribonucleic acid was successfully used to identify genes differentially expressed between normal human brain and malignant glioma tissues. A total of 60 differentially expressed sequences were initially identified, of which 21 were cloned and sequenced. Twenty of the cloned sequences represented novel genes, and one sequence represented a kinesin heavy chain (KHC) gene isoform. The KHC isoform was selected for further characterization. Northern blots of total ribonucleic acid isolated from normal brain and a glioblastoma were probed with our KHC probe and confirmed the differential expression of this gene. Expression analysis of a variety of normal human tissues demonstrated that this KHC isoform is expressed only in brain tissues, with no detectable expression in placenta, spleen, kidney, lung, liver, or skeletal muscle. Our results confirm the rapid and sensitive nature of the differential display technique in identifying differential gene expression. This method offers a means to identify new genes of biological interest in human brain tumors such as oncogenes, tumor suppressor genes, and tumor-specific markers.
Neurosurgery 1995 Sep
PMID:Differential display of messenger ribonucleic acid: a useful technique for analyzing differential gene expression in human brain tumors. 750 Nov 11

Granulocyte-macrophage colony-stimulating factor (GM-CSF) production and receptor expression by human glioblastomas was studied. Enzyme-linked immunosorbent assay showed four of 10 glioblastoma cell lines spontaneously released GM-CSF (2.9-9.2 pg GM-CSF protein/ml culture medium), which was enhanced by stimulation with tumor necrosis factor-alpha (TNF) (10 U/ml) up to 410 pg/ml. TNF also induced secretion of GM-CSF by another cell line. Northern blot analysis identified increasing GM-CSF gene expression by cells following TNF stimulation. However, no GM-CSF protein was detectable in the cerebrospinal fluid of three malignant glioma patients. Intratumoral administration of TNF in the patients also failed to stimulate GM-CSF levels in the cerebrospinal fluid. A binding assay using flow cytometry with biotinylated GM-CSF and Scatchard analysis using 125I-labeled GM-CSF failed to demonstrate GM-CSF receptor expression on the 13 cell lines. Exogenous GM-CSF stimulation had no effect on production of prostaglandin E2, interleukin-6, or interleukin-8 by glioma cells. Human glioblastoma cells secrete GM-CSF without expressing the receptor in vitro, but there was no evidence of GM-CSF production in vivo.
Neurol Med Chir (Tokyo) 1993 Sep
PMID:Human glioblastoma cells produce granulocyte-macrophage colony-stimulating factor in vitro, but not in vivo, without expressing its receptor. 750 98

The infiltration of leukocytes into the central nervous system is associated with many pathologic conditions of the brain. The mechanisms by which these immune cells can penetrate the blood-brain barrier and remain within the brain are not understood. However, elevated brain levels of the pro-inflammatory cytokine IL-1 appear to accompany pathogenesis. The present study provides the first evidence that IL-1 can induce the expression of adhesion molecules for leukocytes on glial cells and suggests a role for the transcription factor NF-kappa B in the induction process. Human rIL-1 alpha was found to induce the expression of the cell adhesion molecules, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) but not E-selectin in human 1321N1 astrocytoma. Both VCAM-1 and ICAM-1 were detectable from 3 h and remained sustained for up to 72 h. Induction was inhibited by the IL-1 receptor antagonist. IL-1 alpha was also shown to induce the expression of VCAM-1 and ICAM-1 in a receptor-dependent fashion in human A172 glioblastoma. Activation of the transcription factor NF-kappa B was also observed in 1321N1 astrocytoma in response to IL-1 alpha treatment and was similarly abolished by pretreatment of cells with antagonist. Activated NF-kappa B was apparent from 20 min and remained for up to 24 h. N-acetylcysteine (NAC) and pyrollidinedithiocarbamate (PDTC), which were shown to inhibit activation of NF-kappa B in Jurkat E6.1 lymphoblasts and EL4.NOB-1 thymoma, failed to block IL-1 activation of NF-kappa B in 1321N1 astrocytoma. However, both of these antioxidants demonstrated complex modulatory effects on the induction of cell adhesion molecule expression by IL-1. The induction of VCAM-1 but not of ICAM-1 proved susceptible to inhibition by both PDTC and NAC. The expression of adhesion molecules for leukocytes on glial cells in response to IL-1 may represent an important mechanism for retention of immune cells in the central nervous system that may be a prologue to inflammatory conditions in the brain.
J Immunol 1994 Sep 15
PMID:Activation of NF-kappa B and induction of vascular cell adhesion molecule-1 and intracellular adhesion molecule-1 expression in human glial cells by IL-1. Modulation by antioxidants. 752 69

A 40-year-old male, treated with radiotherapy and supraophthalmic intracarotid artery (ICA) ACNU infusion for glioblastoma in the right occipital lobe, developed cerebral infarction secondary to vasculopathy manifesting as hemiparesis 3 months after a second ICA injection. The initial diagnosis was focal neurotoxicity, but angiography revealed severe vasospasm of the anterior choroidal artery. The symptoms improved gradually with therapy for the vasospasm. Angiography is required to discriminate vasospasm and focal neurotoxicity as a complication of ICA injection of antineoplastic agents.
Neurol Med Chir (Tokyo) 1994 Sep
PMID:Vasculopathy of the anterior choroidal artery following intra-arterial chemotherapy--case report. 752 54

In primary malignant brain tumors increased vascularity and marked edema strongly suggest a possible role of the vascular endothelial growth factor/vascular permeability factor (VEGF/VPF). This was confirmed by earlier in situ hybridization studies, by analysis of the expression of the mitogen in different subsets of glioblastoma cells, and by the fact that the VEGF/VPF receptor flt-1 (fms-like tyrosine kinase) is up-regulated in tumor cells in vivo. To assess and quantify the expression of the VEGF/VPF gene and of the receptor gene, 26 surgical specimens of brain tumor tissue from 24 patients were analyzed. In most malignant gliomas, the expression level of the VEGF/VPF gene is elevated and can be increased up to 20- to 50-fold in comparison with low-grade tumors. Using polymerase chain reaction-based amplification, it could be shown that the messenger RNAs of three different VEGF/VPF forms are synthesized in tumor tissue samples. Northern blot studies revealed that in some samples a significant expression of the gene coding for placenta growth factor, a growth factor closely related to VEGF/VPF, was observed. In addition, using a radioreceptor assay it was possible to detect high VEGF/VPF-like activity in the cyst fluids of brain tumors, indicating the accumulation of the mitogen and permeability factor in brain tumor cysts. Further investigations revealed that astrocytoma and glioblastoma cells in culture express the VEGF/VPF gene and secrete the VEGF/VPF protein, whereas gene expression of the two known VEGF/VPF receptors, kinase insert domain-containing receptor and flt-1, could not be detected. These data support previous reports, which stated that VEGF/VPF acts as a paracrine growth and permeability factor in brain tumors and may contribute to tumor growth by initiating tumor angiogenesis.
Neurosurgery 1994 Sep
PMID:Detection and quantification of vascular endothelial growth factor/vascular permeability factor in brain tumor tissue and cyst fluid: the key to angiogenesis? 752 59


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