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)

Twenty-two patients, aged 16 to 67, who had malignant gliomas after surgical resection were treated with carmustine and cisplatin intravenous infusion before, during, and after radiotherapy. All patients had subtotal or total resection, or biopsy as the initial procedure. Twenty-one patients who had at least 2 cycles of chemotherapy and finished the whole course of radiotherapy were considered to be evaluable for responses. Among them, 5 had glioblastoma multiforme, 16 had anaplastic astrocytoma. The median time to tumor progression was 35 weeks (range 12-130 weeks) and median survival time was 66 weeks (range 10-156 weeks). Early progression occurred more frequently in patients with biopsy only and subtotal resection, and in patients with glioblastoma than in those with anaplastic astrocytoma. This combined modality treatment program was associated with reversible hematologic toxicity which was severe in 2 patients, and with ototoxicity in 1 patient, nephrotoxicity in 2 patients. Combination of carmustine and cisplatin with cranial irradiation for malignant gliomas is moderately toxic and appears to offer no obvious survival advantage compared with radiation therapy plus BCNU alone.
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PMID:Combination chemotherapy with carmustine and cisplatin before, during, and after radiotherapy for adult malignant gliomas. 859 71

Vascular endothelial growth factor (VEGF) is an angiogenic factor which is known to be expressed in several malignancies including glioma. The effect of transforming growth factor-beta (TGF-beta) isoforms as well as gangliosides on VEGF production was investigated in human glioma cell lines. TGF-beta isoforms and gangliosides were found to differentially stimulate VEGF production by these cells. The ganglioside GD3 enhanced this release to the greatest extent and the stimulation was more marked in a glioblastoma cell line than in the two other anaplastic astrocytoma cell lines. These results suggest that both TGF-betas and gangliosides may act as indirect angiogenic factors by stimulating VEGF secretion.
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PMID:Vascular endothelial growth factor production is stimulated by gangliosides and TGF-beta isoforms in human glioma cells in vitro. 860 72

Vascular endothelial growth factor (VEGF) has been investigated as a potent mediator of brain tumor angiogenesis, vascular permeability, and glioma growth. Using a VEGF ELISA, we determined the concentration of VEGF in the sera and tumor extracts of 19 brain tumor patients including glioblastoma, anaplastic astrocytoma, low grade astrocytoma, meningioma, malignant lymphoma, and metastatic brain tumor as well as normal brain. Although VEGF concentration of the serum was not correlated with that of the tissue, VEGF concentrations of glioblastoma cyst fluid were 200-300-fold higher than those of serum in the patients. VEGF concentration in the tumors was significantly correlated with the vascularity measured by counting vessels stained with von Willebrand factor antibody. VEGF protein localized to the cytoplasm of tumor cells and vasculature in gliomas, predominantly in the peripheral microvessel "hot spots" as well as around the necrosis in glioblastomas. VEGF immunopositivities were well reflected with VEGF concentration determined by ELISA. VEGF ELISA demonstrated time-dependent increase of the VEGF concentration in the serum-free conditioned medium of various glioma cell lines. The conditioned medium with high VEGF concentration induced endothelial cell migration. These observations suggest that VEGF represents a useful marker and measurable element of glioblastoma angiogenesis. The measurement of VEGF concentration by ELISA in tumor and tumor cyst fluid may allow for the assessment of vascularity in gliomas.
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PMID:Concentration of vascular endothelial growth factor in the serum and tumor tissue of brain tumor patients. 861 70

Expression of type IV collagen, fibronectin and laminin in various types of primary human brain tumor sections and normal brain tissue sections as well as cultured glioma cell lines was examined by an immunofluorescence technique. Type IV collagen, fibronectin, and laminin were mainly localized to the basement membrane of the vasculature in glioblastoma, anaplastic astrocytoma, low grade glioma, and in normal brain. However, positive staining for all the extracellular matrix (ECM) components tested was found only in glioblastoma sections both in the cells and in the ECM. In all other tumor types and in normal brain tissue, the cells did not stain for any of the ECM components. Four glioblastoma cell lines and autologous ECM synthesized by respective glioblastoma cell lines also showed positive staining for type IV collagen, fibronectin and laminin in vitro. These results suggest that glioblastoma cells both in vitro and in vivo express the extracellular matrix components that are involved in the regulation of tumor cell invasion.
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PMID:Immunohistochemical localization of extracellular matrix proteins in human glioma, both in vivo and in vitro. 862 73

Proteinases and their inhibitors may play a role in the development and progression of many cancers. Several studies suggested that lysosomal proteinases cathepsin B, L, and D may be involved in the malignant progression of some human neoplastic diseases. In this study, we determined the levels of cathepsin H in human glioma progression and the significance of cathepsin H in glioma cell invasion. Levels of cathepsin H antigen were found to be significantly higher in glioblastomas and anaplastic astrocytoma when compared with normal brain tissue and low-grade gliomas. Western blotting confirmed the presence of authentic cathepsin H with a doublet at 27 and 25 kDa in normal brain tissue and tumor samples. However, the intensity of the band increased significantly in glioblastoma samples. Cathepsin H antibody inhibited the invasion of glioblastoma cell lines through Matrigel invasion assay. These data suggest that the tumor-specific increase in antigen may be a useful independent marker of tumor progression in central nervous system neoplasms.
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PMID:Expression and the role of cathepsin H in human glioma progression and invasion. 864 Jul 38

We present the results of a retrospective survey of 1,218 patients treated at the Norwegian Radium Hospital during the years 1980-94 for primary tumours of the central nervous system. Median survival for patients with glioblastoma (n = 492) was 12 months, for patients with anaplastic astrocytoma (n = 83) 25 months, astrocytoma (n = 260) 95 months, oligodendroglioma (n = 85) 74 months, mixed glioma (n = 68) 65 months, and medulloblastoma (n = 53) 109 months. Median survival for patients with brain stem tumours (n = 37) was nine months, while 74% of patients with tumours in the pineal region (n = 38) survived for five years. The histology and localisation of the tumour, as well as age and functional status, are important prognostic factors for survival in patients with primary CNS tumours.
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PMID:[Prognosis in primary tumors of the central nervous system. A patient material from the Norwegian Radium Hospital 1960-94]. 865 12

P53 immunohistochemistry in astrocytic tumors has usually been evaluated by the percentage of positive cells. However, in this study we analyzed the P53 immunopositive cells by their patterns of distribution. Formalin-fixed and paraffin-embedded sections from 38 patients with astrocytic tumors were examined. The distribution pattern of P53 immunostaining cells was divided into 3 types: negative, locally scattered, and diffuse clustering. There were 2 positive stains in 5 astrocytomas (40%), 12 positive in 24 anaplastic astrocytomas (50%), and 7 positive in 9 glioblastoma multiformes (78%). In astrocytomas, the positive cells were locally scattered. In anaplastic astrocytoma and GBM, the positive cells appeared locally scattered or as diffuse clustering. For the variant immunoreactive expression, the mean ages for patients with negative, locally scattered and diffusely clustered P53 immunostaining were as follows: 51.4, 52.6, and 28.4 years (P < 0.01), respectively. In anaplastic astrocytoma and GBM, the diffusely clustered pattern was more common in younger patients, whereas elderly patients in same groups tended to have few or no P53 immunopositive cells. Thus, our results implicate that clonal expansion of P53 immunopositive cells is associated with brain tumor progression.
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PMID:Immunohistochemical pattern of P53 protein in human astrocytic tumors. 867 33

The most important prognostic factor in malignant gliomas is histopathological diagnosis of the tumor. The survival of patients with anaplastic astrocytoma is much longer than that of patients with glioblastoma. The median survival of the former has been improved up to almost 4 years by the recent progress of multidisciplinary treatment, whereas that of the latter has still remained in less than 1.5 years. Other important factors proved to be associated with survival of patients with malignant gliomas are the age of patients, Karnofsky performance status on admission, surgery, radiotherapy and chemotherapy. There is substantial evidence suggesting an association between younger patient age and longer survival in adults with supratentorial anaplastic astrocytoma as well as glioblastoma. It is also consistent with evidence that the patients with better performance status on admission live longer after treatment. Gross total resection of supratentorial anaplastic astrocytoma is directly associated with longer and better survival when compared to subtotal or partial resection. For glioblastoma, however, gross total resection has not been proved to have a significant survival advantage over subtotal or partial removal. Radiotherapy has been proved to be associated with longer survival of patients with supratentorial anaplastic astrocytoma and glioblastoma. Chemotherapy has not proved effective in prolonging the survival of patients with glioblastoma. Multidrug chemotherapy with CCNU, procarbazine and vincristine has proved to have significant survival advantage over BCNU alone, suggesting chemotherapy is also a prognostic factor in patients with anaplastic astrocytoma.
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PMID:[Prognostic factors in malignant gliomas]. 867 27

Recent studies suggest that aspartic proteinase cathepsin D may be implicated in tumor invasion and metastasis either directly by degrading extracellular matrix or indirectly by activating the cysteine proteinases such as procathepsin B, H, and L to mature forms or by inactivating cysteine proteinase inhibitors. In this study we determined for the first time whether increased levels of cathepsin D correlate with glioma progression by enzymatic assay, ELISA, and western blotting. Cathepsin D activity and content were higher in anaplastic astrocytoma and in glioblastoma tissue extracts especially when compared to normal brain tissue and low-grade gliomas. There was a significantly increased intensity of an M(r) 29,000 band in glioblastoma and anaplastic astrocytoma compared to low-grade glioma and normal brain tissue on Western blotting analysis using its specific antibodies. Cathepsin D antibody inhibited the invasion of glioblastoma cell lines in a dose-dependent manner. These results suggest that the expression of cathepsin D is dramatically upregulated in malignant gliomas, and that its increase correlates with the malignant progression of human gliomas in vivo.
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PMID:Expression of cathepsin D during the progression of human gliomas. 873 97

Human astrocytoma cells were studied using whole-cell patch-clamp recording. Voltage-dependent outwardly-rectifying anion currents were identified in primary cultures of six freshly resected human brain tumors and in seven established anaplastic astrocytoma/glioblastoma cell lines (U251MG, CH235MG, U373MG, U105MG, D54MG, SK-MG-1, and STTG1). Anion currents were not observed in normal, non-neoplastic glial cells, nor in human tumor-derived cells of non-glial origin (melanoma, breast cancer, neuroblastoma, rhabdomyosarcoma). Currents activated at potentials > 50 mV and showed large transients upon termination of voltage steps. Currents reversed at the predicted equilibrium potential for chloride ions and could also be recorded when Cl- was replaced by F-, Br- or I-. Currents were inhibited by the Cl- channel blockers chlorotoxin, DIDS, and DNDS. These Cl- currents may play a role in the growth control of astrocytoma cells.
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PMID:Human astrocytoma cells express a unique chloride current. 874 85


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