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)

Ten patients with brainstem tumors (BST) underwent Gamma Knife radiosurgery. In 5 cases, there were definitive histological diagnoses; ependymoma (n = 3) and CNS lymphoma (n = 2). The others were diagnosed as ependymoma (n = 1), CNS lymphoma (n = 2) and glioma (n = 2) on clinical grounds. Of 4 cases with ependymoma, the tumor showed a marked response in 3 cases. Of 4 cases with CNS lymphoma, all responded rapidly and the clinical symptoms improved markedly. However, in the 2 cases with glioma, the tumor remained unchanged or continued to grow. Gamma Knife radiosurgery was effective in local growth control of BST without adverse effects. An alternative treatment design will be required in glioma cases.
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PMID:Gamma Knife radiosurgery for the treatment of brainstem tumors. 858 38

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

11C-methyl-L-methionine (C-11 Met)PET, CT and MR imaging were performed in eleven patients with malignant brain tumors before and after RT to evaluate the usefulness of positron emission tomography (PET) in monitoring tumor response to radiotherapy (RT). The subjects included five cases of intracranial malignant lymphoma (ICML) and six cases of glioma. C-11 Met uptake by the tumor (T) and the contralateral gray matter (NT) was calculated on the PET images. The mean T/NT ratio of the ICMLs and gliomas changed from 2.33 and 1.87, respectively, before RT to 1.31 and 1.58, respectively, after RT.No significant difference was found between the T/NT ratios before and after RT in either the ICMLs or the gliomas (t-test). We tentatively defined the minimum T/NT ratio, 1.2, as the threshold between tumor and nontumor regions. Tumors with a ratio of 1.2 or more were imaged as "hot" (MET) and coincided with CT or MR image lesions which were visualized as contrast-enhancing (CE) and low-density (LD) or high-intensity (HI). The relationships between PET, CT and MRI lesions were classified as follows: Type I (MET < or = CE), Type II [CE < MET < LD (HI)], Type III [LD(HI) < or = MET]. MET lesions extending regionally ( > 1 cm) beyond the respective CT or MR image lesions were designated "MET-extension" and LD (HI) lesions protruding ( > 1 cm) beyond the MET lesions were recorded as "LD (HI)-extension" on the integrated images. The type II pattern of the MET areas in all five cases of ICML before RT had changed to Type I in one case, Type III in one case and Type II in three cases, after RT, while the two Type II patterns and four Type III patterns of the gliomas had converted to four Type II and two Type III patterns. These findings indicate that gliomas tend to invade into areas of peritumoral edema more than ICMLs. There were two ICML MET-extension sites in the cortex before RT, as opposed to two in the cortex, one in the basal ganglia, one in the thalamus, and one in the corpus callosum among the gliomas. On follow-up CT or MR images MET-extension (75%) had converted to a CE or LD (HI) region. Four ICML LD (HI)-extension sites before RT were found in periventricular white matter, versus one in the cortex and three in the white matter among the gliomas. LD (HI)-extension appeared to represent vascular edema because it decreased or diminished after completion of therapy. Sequential analysis of integrated C-11 Met PET, CT and MR images is useful in detecting the extent of tumor infiltration by ICMLs and gliomas, particularly at an early stage, and for evaluating the effect of RT in the treatment of both.
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PMID:[Sequential analysis of the integrated images of PET, CT and MR in malignant brain tumors before and after radiotherapy]. 867 4

The role of inflammatory reactions in brain tumors is still unclear. In particular, there is little information about the participation of the microglia/macrophage cell system. We therefore investigated 72 surgical biopsy samples of brain tumors (astrocytoma, glioblastoma, oligodendroglioma, ependymoma, medulloblastoma, cerebral lymphoma, gangliocytoma, neurocytoma and germinoma) and the brains of eight cases with malignant gliomas that came to autopsy, using immunohistochemical markers for the monocyte/macrophage lineage (Ki-M1P, HLA-DR, KP1, My4, My7, Ki-M1, Ki-M6, EBM 11). These markers allowed us to characterize four subtypes of the microglia/macrophage cell system: ramified microglia, ameboid microglia, perivascular microglia and brain macrophages. Among the different tumors, glioblastomas and anaplastic gliomas showed the largest number of mixed cell populations, which consisted of macro-phages and ramified and ameboid microglia. In glial tumors of low malignancy fewer, predominantly ameboid, microglia were found. Neuronal tumors showed only a mild increase of microglia. Cerebral lymphomas contained macrophages diffusely distributed within the tumor center, while activated microglia were prominent at the border zone and in the adjacent brain tissue. The autopsy cases were used to study the morphometric distribution of microglia/macrophages. There was a significant increase of microglia/macrophages within the tumor, but no differences were seen between central and peripheral tumor areas. The non-neoplastic gray and white matter contained more microglial cells than controls. We conclude that the distribution pattern of ameboid and ramified microglial cells and macrophages is distinct in most of the investigated tumor types, underlining the complex immunological function of the microglia/macrophage cell system.
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PMID:Distribution and characterization of microglia/macrophages in human brain tumors. 887 Aug 31

Water-soluble metabolites extracted from 60 surgically excised samples of various brain tumors and four nontumorous lobectomized brains were measured quantitatively using in vitro high-resolution magnetic resonance spectroscopy. A detailed MR spectrum-histology correlation study in a glioblastoma was made, to reveal MR spectral changes in accordance with the density of glioma cells. Furthermore, three cases that had difficult preoperative diagnoses are discussed. MR spectra from gliomas exhibited characteristic patterns according to malignancy, presumably reflecting its metabolic effects. Concentrations of choline-containing compounds, inositol, alanine, glycine and phosphorylethanolamine (PEA) increased according to the degree of malignancy, but it was noteworthy that in glioblastoma the choline-containing compounds, inositol, alanine, glycine and phosphorylethanolamine increased according to the degree of malignancy. In particular, the glycine concentration was very high in glioblastoma. We also detected a large amount of taurine in medulloblastoma. Although the total creatine concentrations decreased according to the malignancy, the concentration of total creatine was relatively preserved in neuroectodermal tumors but was low in nonneuroectodermal tumors. N-acetyl-aspartate was unequivocally demonstrated in normal tissues, but could not be detected in nonneuroectodermal brain tumors such as metastatic brain tumor, meningioma, neurinoma and chordoma. In meningioma, although a high peak of choline-containing compounds has been reported uniquely by in vitro and in vivo 1H-MRS, we demonstrated that its concentration was not increased in meningioma; instead, there was an increased alanine content. 1H-MRS of neurinoma demonstrated high inositol peaks, and a large amount of inositol. The reason for the high inositol content in neurinoma is unknown, but the prominent peak of inositol on MR spectra should be useful for the differential diagnosis of neurinoma from meningioma. PEA concentration was increased four to five times in pituitary adenoma, malignant lymphoma, and medulloblastoma as compared with normal brain. Thus 1H-MRS might provide clinically useful information on tumor malignancy and characteristic tumor metabolism. Although excellent anatomical information of tumors can be readily obtained by magnetic resonance imaging. MRS provides metabolic information. MRS may provide additional information in cases in which the differential diagnosis of tumors by neuroimaging is difficult.
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PMID:Absolute concentrations of metabolites in human brain tumors using in vitro proton magnetic resonance spectroscopy. 925 Nov 9

Mature T cells are susceptible to activation-induced cell death in the periphery. Activation-induced cell death is thought to involve CD95/CD95 ligand interactions in vivo. Here we report that stimulated, CD45RO+ human T cell lines specific for myelin basic protein or tetanus toxoid from multiple sclerosis patients and healthy individuals resist apoptosis induced by soluble recombinant CD95 ligand in vitro. In contrast, the same CD95 ligand effectively kills Jurkat T lymphoma and human malignant glioma cells. The resistance of the T cell lines is not due to a lack of CD95 expression at the cell surface and is not overcome by coexposure to CD95 ligand and inhibitors of RNA or protein synthesis. The expression level of BCL-2 is lower in Jurkat than in Ag-specific T cells. After exposure to soluble CD95 ligand, Jurkat T cells, but not Ag-specific T cells, exhibit loss of BCL-2 and BCL-X expression whereas BAX expression is not affected. Surprisingly, Ag-specific T cells are rather sensitive to CD95 ligand expressed at the cell surface of N2A neuroblastoma cells. Accessory molecules expressed by the CD95 ligand-expressing effector cell are dispensable for apoptosis since the T cells are equally sensitive to agonistic APO-1 Ab. Further studies are required to determine whether resistance to soluble CD95 ligand-mediated apoptosis is a possible escape mechanism for T cells from peripheral deletion that may have relevance for autoimmune disorders.
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PMID:Human autoreactive and foreign antigen-specific T cells resist apoptosis induced by soluble recombinant CD95 ligand. 927 96

This review is made up of two parts. The first section describes techniques and methods used in the treatment of malignant brain tumors, stressing the most recent developments. The second part reviews the therapeutic modalities in malignant gliomas, where an attempt is made to consider separately glioblastomas, anaplastic astrocytomas and oligodendrogliomas, low-grade glioma, medulloblastoma, primary brain lymphoma, and brain metastases. A decision making algorithm is suggested for each tumor type.
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PMID:Management of malignant brain tumors. 936 37

A 2.5 kb human cDNA clone containing a CAG trinucleotide repeat, designated HB20, was isolated from a human fetal brain library. Northern analysis on multi-tissue blots and various cell lines confirmed that HB20 is specifically expressed in the brain. Its expression is low in two glioma cells, moderate in a neuron precursor cell, NT2, but absent in lymphoma, cervical carcinoma, or colonic carcinoma cells. Significant increase of HB20 mRNA was shown along with retinoic acid-induced terminal differentiation of NT2 cells into neuron cells, hNT. Homology comparison of the predicted HB20 amino acid sequence with the current database revealed that it belongs to a newly recognized protein family composed of nucleosome assembly proteins and SET proto-oncogene, which has been shown to interact specifically with B-type cyclins involved in the control of cell proliferation. Together with the detection of nuclear localization signals and apparent nuclear distribution of expressed protein, HB20 is likely to be a brain-specific nuclear protein, functioning in the process of neuronal differentiation.
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PMID:Molecular cloning and characterization of a human brain-specific gene implicated in neuronal differentiation. 952 61

Immunohistochemistry (IHC) has provided major insights about the classification of brain tumors by identifying cellular markers of phenotype and about tumor growth potential with nuclear markers of proliferation. In situ hybridization (ISH) research shows promise for diagnostic applications in tumor classification. The avidin-biotin conjugate IHC procedure is highlighted for diagnostic use on routinely processed clinical specimens. The immunophenotypes of brain tumors are tabulated in reference to their common IHC markers. Tumors that have been correctly classified by their IHC phenotypes include the giant-cell glioblastoma, primary brain lymphoma, and central neurocytoma. Phenotypes that may be more definitively detected by ISH, such as pituitary hormone, immunoglobulin light chain, and collagen messages are described. IHC of nuclear proliferation markers correlates with grade of malignancy, predicts tumor growth potential, and is prognostic for patient survival. The incorporation of bromodeoxyuridine, the expression of proliferating cell nuclear antigen, and the expression of Ki-67 antigen detected by MIB-1 antibody are compared in regard to their cell cycle activity and labeling index determinations. Fluorescence in situ hybridization (FISH) of brain tumor interphase nuclei and chromosomes is described. Abnormal FISH signals of specific chromosomes are associated with different types of brain tumors, with different grades of malignancy, and with mesenchymal drift of glioma cells in culture.
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PMID:Insights about brain tumors gained through immunohistochemistry and in situ hybridization of nuclear and phenotypic markers. 960 6

Chemotherapy delivery for the treatment of malignant brain tumors is markedly enhanced when given in conjunction with osmotic opening of the blood-brain barrier. Osmotic opening or disruption of the blood-brain barrier is achieved while the patient is under general anesthesia, by the infusion of mannitol into the internal carotid or vertebral artery circulation. The mannitol infusion is followed by administration of intraarterial chemotherapy. A National Blood-Brain Barrier Program now exists and includes six universities. Within the National Program over 4200 blood-brain barrier disruption procedures have been performed in over 400 patients. Patients with primary central nervous system (CNS) lymphoma, glioma, primitive neuroectodermal tumor (PNET), germ cell and metastatic cancer are eligible for treatment. Results in patients with primary CNS lymphoma, recently reported in the Cancer Journal, include the first example of a durable response in a primary brain tumor without loss of cognitive function and without use of radiotherapy. Results with PNET and germ cell tumors are also very encouraging. Advanced practice nurses coordinate the care of blood-brain barrier disruption patients. Care includes patients selection, education, close neurological observation, maintenance of fluid and electrolyte balance and managing effects of high-dose chemotherapy. Both acute and long-term medical and psychological follow-up are an essential component of the program, as well as patient and family support.
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PMID:Blood-brain barrier disruption for the treatment of malignant brain tumors: The National Program. 964 16


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