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)

Monoclonal antibodies (mAbs) recognizing the disialoganglioside II3(NeuAc)2GgOse3Cer (GD2) were produced by immunizing mice with the GD2-expressing neuroblastoma cell line LAN-1 and a prefusion boost with purified GD2 coupled to Salmonella minnesota. Two IgM mAbs were isolated which demonstrated high levels of reactivity (binding ratios in excess of 100) with GD2 by solid-phase radioimmunoassay and positivity in high-performance thin-layer chromatography (HPTLC) immunostain; only one (DMAb-20) was subsequently shown by analysis with a panel of defined ganglioside species to be specific for the minimum epitope of GD2 GalNAc beta 1-4(NeuAc alpha 2-8-NeuAc alpha 2-3)Gal-, DMAb-20 was used to evaluate the expression of GD2 by malignant glioma and medulloblastoma cell lines using cell surface radioimmunoassay. indirect membrane immunofluorescence. HPTLC immunostain, and densitometric analysis of extracted gangliosides from selected cell lines. Sixteen of 20 (80%) malignant glioma and 5 of 5 medulloblastoma cell lines reacted with DMAb-20; in agreement with previous studies, 5 of 5 neuroblastoma and 2 of 3 melanoma cell lines also reacted with DMAb-20, GD2 was proportionally increased in the glioma and medulloblastoma cell lines relative to levels in normal brain, as determined by densitometric analysis. In a phenotypic survey of malignant glioma biopsies, tumor cells in 24 of 30 (80%) cases stained positively with DMAb-20. Reactive astrocytes, both within the adjacent to tumors, were frequently intensely stained. Among the morphological variants of glioblastoma examined, the most intense staining with DMAb-20 was observed in neoplastic gemistocytes, with the weakest or absent staining in small cell glioblastomas. As GD2 is a commonly expressed surface antigen of gliomas and medulloblastomas, expression of which is retained in tissue culture. DMAb-20 will be useful in determining the functional role of GD2 in cell-cell interaction, adhesion, and invasion, and in defining altered growth control mechanisms of central nervous system neoplasms in in vitro models.
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PMID:Disialoganglioside GD2 in human neuroectodermal tumor cell lines and gliomas. 165 6

Using DAPI-DNA cytofluorometry, the author analyzed nuclear DNA content of formalin fixed, paraffin embedded, glioma material obtained from 14 glioma cases at surgery. Sections of 10 microns were deparaffinized. Following simultaneous DAPI (4,6-diamidino-2-phenylindole dihydroporphyrin chloride)/HP (hematoporphyrin) staining, DAPI binds DNA and DNA-DAPI complexes emit blue fluorescence when exited by ultraviolet (UV) light. Through Zeiss fluorescence microscope, the author measured nuclear fluorescence intensity with histological verification of glioma cells. A DNA histogram was obtained with fluorescence intensity recorded on the abscissa and number of cells plotted on the ordinate. Samples of 20 normal non-neoplastic astrocytes taken from apparently normal brain tissue included in the histological slide were used as diploid (2 C) control. Based on DNA content, tumor cells were classified into 4 groups: N-group composed of cells with 2 C DNA content (normoploid), S-group with less than 2 C (hypoploid), L-group more than 4 C (hypertetraploid), I-group between 2 C and 4 C (intermediate ploidy). Intermediate ploidy was significantly higher and normoploid was significantly lower in glioblastoma compared with those of benign astrocytoma. Thus, DNA content and histological malignancy were well correlated. Due to limitation of measuring diaphragm of turret in the microscope, some extra large cell could not be included in it and was excluded from the measurement.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[DAPI-DNA cytofluorometric study of glioma cells--application of DAPI-DNA cytofluorometry to paraffin embedded archival glioma tissue for nuclear DNA content analysis]. 169 81

Three cases of multiple gliomas with postmortem findings including a rare case of multicentric glioma are presented. A 59-year-old female was hospitalized with decreased mental activity and gait disturbance. Computed tomographic (CT) scans and magnetic resonance (MR) images showed two independent mass lesions in the left frontal and the right temporal lobes, shown by postmortem to have no communication. Histologically, they were a gemistocytic astrocytoma and an anaplastic astrocytoma, respectively. Therefore, multicentric glioma was diagnosed. A 66-year-old male was admitted with slow mentation and gait disturbance. CT scans and MR images demonstrated two mass lesions; one overriding the bilateral frontal lobes through the corpus callosum and the other in the left temporal lobe. Postmortem examination showed that both lesions were glioblastoma and the left temporal tumor was accompanied by subarachnoid dissemination. A 29-year-old male was hospitalized with gustatory hallucination and convulsions of the right upper extremity. CT scans revealed two mass lesions in the right frontal and the left temporal lobes. MR images demonstrated communication between the two lesions through the corpus callosum. The left temporal tumor developed into the occipital lobe and another new lesion appeared in the right temporal lobe despite chemotherapy and irradiation. Postmortem examination revealed communication between the three masses through the corpus callosum. Histologically, all three tumors were glioblastoma. Multicentric gliomas have been reported at various incidences from 2.3 to 9.1%. However, multicentric gliomas with multiple tumors of different histologies are very rare and only 16 cases have been reported. MR imaging is more valuable than CT scanning to detect communication between two or more lesions.
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PMID:Clinicopathological study of multiple gliomas--report of three cases. 170 39

The human glioblastoma-derived cell lines 86HG-39, 87HG-28 and 87HG-31, used for the production of monoclonal antibodies (mAbs) against glioma-associated antigens (GAA), were characterized in terms of morphology, growth behaviour, chromosomes and antigen expression. In the primary tumours, differential expression of glial fibrillary acidic protein, S100 protein, Leu-7 and GAA as defined by mAbs MUC 2-39, MUC 2-63 and MUC 8-22 was demonstrated. Receptors for epidermal growth factor (EGFr) and nerve growth factor (NGFr) were found in many cells in short-term cultures, but the transferrin receptor (Tr) was found in only a few cells of 87HG-28. In permanent cell lines, differentiation antigens and EGFr decreased and Tr increased markedly. NGFr and GAA remained stable. Transplantation tumours of 86HG-39 were partly positive for Tr and GAA. Chromosomal analysis revealed that the 86HG-39 and 87HG-28 cell lines had a hypodiploid or diploid stem line with lines in the hypotetraploid to tetraploid region for 50 in vitro passages. The 87HG-31 cell line had chromosomal patterns in the hypotriploid to triploid region. A gain of chromosomes was seen in the groups C7, C8, C10, D14, F19, F20, G21, G22. The variability of antigens in these tumours and especially during long-term cultivation probably reveals an ability to influence the growth of malignant glioma cells via the respective effector molecules.
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PMID:Morphological, immunocytochemical and growth characteristics of three human glioblastomas established in vitro. 170 26

Immunohistochemistry was performed on paraffin sections from human glioblastoma multiforme and normal brain tissue. Acidic fibroblast growth factor (FGF) was abundantly present in astrocytes from all glioblastomas studied. Basic FGF was found in the matrix surrounding proliferating blood vessels in most of the glioblastomas. In contrast, astrocytes from normal brain did not contain acidic FGF, and perivascular matrix staining was not demonstrated for basic FGF in the normal brain. Both growth factors could be demonstrated in neurons, Purkinje cells, capillary endothelium, and arterial walls in the normal brain. This study implicates both growth factors in the pathogenesis of malignant glioma. Both may be significant mediators of angiogenesis in glioblastoma.
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PMID:Acidic and basic fibroblast growth factors are present in glioblastoma multiforme. 171 53

Cis-diamminedichloroplatinum (CDDP) was administered by selective continuous internal carotid infusion to nine patients with malignant brain tumors, including five glioblastomas, one mixed glioma, and three metastatic tumors. CDDP was infused through a catheter in the internal carotid artery at 100 mg/hr in all cases, except one glioblastoma case in which the lower rate of 10 mg/hr was used. The results of CDDP concentration measurements were: 1) CDDP in the blood peaked at termination of CDDP infusion and then decreased slowly, 2) CDDP infiltrated intratumoral cysts and accumulated there, 3) CDDP in the cerebrospinal fluid peaked 6-18 hours after infusion, and 4) the tumor/plasma CDDP ratio varied from 2 to 8. The size of tumors decreased moderately in three of the nine cases, but no complete response was achieved. The histological changes due to CDDP were observed in the tumor tissue and were absent in the normal brain parenchyma.
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PMID:Pharmacokinetic study of selective continuous internal carotid CDDP infusion in malignant brain tumors. 172 56

The effects of trapidil on platelet-derived growth factor (PDGF)-associated growth of glioblastoma cells were studied. The assessment using PDGF-dependent rat lung endothelium cells revealed secretion of a PDGF-like factor from SF-126 cell line but not from SF-188. Human recombinant PDGF stimulated proliferation of both these glioblastoma cell lines. The anti-PDGF monoclonal antibody inhibited the growth of SF-126 more than SF-188. The results suggest the presence of an autocrine growth mechanism in SF-126 cells mediated by PDGF. The growth of both SF-126 and SF-188 cells was suppressed by trapidil, a specific PDGF antagonist, at 10 and 50 micrograms/ml, respectively. The proliferative response to exogenous PDGF and the antagonistic effect of trapidil were greater in the SF-126 cell line. In addition, trapidil markedly reduced production of prostaglandin E2 in both glioblastoma cell lines. This anti-proliferative effect on malignant glioma cells suggests that trapidil might be a new therapeutic agent for malignant gliomas.
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PMID:Antiproliferative effect of trapidil on PDGF-associated growth of human glioma cell lines in vitro. 172 94

The relationship between the thermosensitivity of cultured brain tumor cells and cytoskeleton was studied. C6 rat glioma cell line (C6 cells) and U-373-MG human glioblastoma cell line (MG cells) were used in monolayer culture. Survival rates at various temperatures were calculated by colony forming assay 10 days after heat treatment. Actin filaments, the main components of microfilaments, were observed by the 7-chloro-4-nitrobenzo-2-oxadiazole phallacidin staining and indirect immunofluorescence staining methods. Alpha-tubulins, the main components of microtubules, were also stained with an indirect immunofluorescence staining method. The morphological changes were investigated by scanning electron microscopy (SEM). Both the C6 cells and the MG cells showed moderate thermosensitivity on the survival curves. Actin filaments were revealed at stress fibers and the ruffles of the leading edge on both cell lines. Stress fibers were well developed in MG cells but were only minor in C6 cells. After heat treatment ruffles and stress fibers were disrupted. However, alpha-tubulins were not affected by heat treatment. SEM showed Swiss-cheese like change of cell surfaces due to many pores with disruption of ruffles and stress fibers after heat treatment. These results suggest that the cytoskeleton, especially microfilaments, may be damaged by hyperthermia.
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PMID:[Thermosensitivity of glioma cells with special reference to changes in cytoskeletons]. 172 43

Interstitial irradiation is a promising treatment for malignant glioma. Longer than expected survival periods following treatment of recurrent tumor have led to the use of brachytherapy as an adjuvant treatment. The impact of patient selection on survival data was studied among candidates for this therapy. Consecutive, conventionally treated adults with newly diagnosed supratentorial tumors were identified retrospectively at a center where experience with glioma is population-based. Based on imaging and performance status, two surgeons and a radiation oncologist designated each patient as either eligible or ineligible for adjuvant brachytherapy. The survival and prognostic factors in the eligible and ineligible groups were analyzed. Overall, the patients eligible for brachytherapy (32% of the series) lived significantly longer than the ineligible patients (16.57 vs. 9.30 months), were younger, and had larger resections and better function. For glioblastoma, 40% of patients were eligible, and lived much longer than those who were ineligible (13.90 vs. 5.80 months). It is concluded that better outcome following adjuvant brachytherapy for glioma is at least in part the result of patient selection. Randomized trials of comparably selected patients will be necessary to demonstrate conclusively that longer survival is also a result of treatment.
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PMID:Selection bias, survival, and brachytherapy for glioma. 173 Sep 45

Expression of major heat shock and stress-induced protein, HSP70, is known to be under complex regulation in tumor cells. In this study, we investigated the alternations of cytokinetics and HSP70 expression by hyperthermia in the in vitro experimental systems, using two rat glioma cell lines, two human glioblastoma cell lines and rat glioblast cells. For hyperthermal treatment the flasks were placed in water baths warmed up at 41 -45 degrees C for 15 min. To determine the effect of hyperthermia on the cell cycle progression, the changes in the DNA distribution of the cell population were studied by flow cytometry (FCM). The levels of HSP70 protein were determined by immunoblot analysis. The relationship between cell cycle and HSP70 expression was investigated by FCM using PI and FITC-labelled HSP70 double staining technique. These results were as follows: 1) Compared with the control, hyperthermic treatment at 42 degrees C or 44 degrees C caused both 354A and T98G cells to accumulate in S phase 18 hours after treatment and G2/M phase after 6-18 hours. 2) Hyperthermic treatment at 42 degrees C caused C6 cells to accumulate in S phase 6 hours after treatment, whereas heat treatment at 44 degrees C caused C6 cells to accumulate in S phase after 18 hours and G2/M phase after 6 hours. 3) A172 cells were accumulated only in G2/M phase by hyperthermia. 4) Glioblast cells did not show the alterations of cytokinetics by heat treatment remarkably. 5) HSP70 protein synthesis were enhanced under hyperthermic conditions in all type of cells, whether primary glioblast or permanent glioma cell lines.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Alterations in cytokinetics and heat shock protein (70 kDa) expression of glial cell by hyperthermia]. 174 92


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