Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 26-year-old woman presented with headaches, incoordination and a cerebellar mass (1982). The CT scan revealed dilated ventricles and a hypodense space-occupying lesion adjacent to the fourth ventricle. Neuronal loss, gliosis and masses of Rosenthal fibers were seen in biopsy. There was no evidence of neoplasm. A second biopsy 2 years later was similar to the original specimen. A diagnosis of Alexander's disease was suggested. Later that year the patient's 11-year-old brother manifested a clinical picture initially diagnosed as brainstem glioma, but whose biopsy was characteristic of Alexander's disease. There has been a gradual deterioration of these siblings over the past 6 years (1986-1991). No evidence of neoplasm has appeared.
 ...
PMID:Biopsy diagnosis of familial Alexander's disease. 145 72

Ethanol inhibits opioid peptide binding to the delta-opioid receptor. When neuroblastoma x glioma NG108-15 hybrid cells are grown with 25-200 mM ethanol, opioid receptor density increases up to 2-fold without a change in receptor affinity. Since changes in neurotransmitter receptor density may be important in neuronal adaptations to ethanol, we investigated the underlying mechanisms and functional consequences of this phenomenon. The opiate antagonist, naloxone, also increased opioid receptor number, but produced a smaller effect than ethanol with greater fractional inhibition of binding; long term enhancement of binding by ethanol is therefore not a simple function of acute receptor inhibition. Ethanol did not inhibit receptor down-regulation by etorphine, an opiate agonist, and therefore is not likely to increase receptor expression through interference with tonic down-regulation by endogenous opioid peptides. Ethanol increased opioid receptor expression in NG108-15 cells treated with actinomycin D, but not cycloheximide; hence, normal protein synthesis, but not DNA transcription, may be required for this response. The opioid receptors induced in ethanol-treated cells were subject to normal up-regulation by naloxone, down-regulation by etorphine, and acute inhibition of agonist binding by Na+. Etorphine maximally inhibits cyclic AMP accumulation in NG108-15 cells with only fractional occupancy of opioid receptors. Chronic ethanol exposure increased the receptor reserve for this response, resulting in a 3.5-fold increase in the potency of etorphine for inhibiting phenylisopropyladenosine-stimulated cyclic AMP accumulation. Neuronal adaptation to ethanol may involve changes in the density of receptors that regulate cellular levels of cyclic AMP.
 ...
PMID:Ethanol increases the expression of functional delta-opioid receptors in neuroblastoma x glioma NG108-15 hybrid cells. 300 82

Neuronal factors from conditioned medium of neuroblastoma X glioma hybrid cells or isolated from embryonic pig brain aggregate acetylcholine receptors (AChR) on cultured chicken and rat myotubes. A membrane surface protein labelled with a fluorescent monospecific antibody was not aggregated with the same treatment. Antibodies against AChR block the action of the aggregating factors but do not produce large aggregates themselves. These findings indicate that the factors specifically react with the AChR on developing myotubes.
 ...
PMID:Specificity of neuronal factors which aggregate acetylcholine receptors on cultured myotubes. 388 36

The relative susceptibility of neurons and glia, grown as monolayers in vitro, to rabies virus infection was explored. Established cell lines of neuronal or glial phenotype and primary cultures of cells derived from mouse dorsal root ganglia (DRC) or brain were used as homologues of the targets of rabies virus in the nervous system. Fixed rabies virus (CVS) strain was used in most experiments; other fixed rabies strains (PV, HEP, ERA) and a street rabies virus isolate were used in some. Virus-cell tropism was determined by immunofluorescence assay for rabies nucleocapsid antigen and cell permissivity was assessed by titration of virus yields. Neuronal cells always exhibited a much greater susceptibility to infection and a greater propensity to sustain viral growth. By immunofluorescence, 90-100% of neurons commonly had viral inclusion bodies, while doses of the virus three to four orders of magnitude higher still left greater than 99% of astrocytes, in brain cell cultures and 90 +/- 5% of the non-neuronal cells in DRG cultures without any obvious signs of rabies virus. Neuroblastoma cells (95 +/- 5% with viral antigens) produced viral yields about four orders of magnitude higher than glioma cells (10 +/- 5% with viral antigens). Though the overall infectivity of street virus was lower than that of fixed virus strains, a significantly higher viral tropism for neurons than for glia was maintained. Thus, primary neuronal cultures offer a means of exploring molecular events in rabies virus infection and their role in pathogenesis.
 ...
PMID:Neurotropism of rabies virus. An in vitro study. 686 37

Recent studies showed that the Alzheimer amyloid precursor (APP) occurs as the core protein of a chondroitin sulfate proteoglycan (appican) in C6 glioma cells. In the present study we show that appican is present in both human and rat brain tissue. Cortical rat brain cell cultures were used to identify appican-producing cells. Soluble secreted and cell-associated appican was produced by mixed glial cultures but not by primary neuronal cultures. Among the three major glial cell types, astrocytes produced high levels of appican, while oligodendrocytes failed to produce any. Only low levels of this molecule were occasionally detected in microglial cultures. Expression of appican in astrocyte cultures was regulated by the composition of the growth media. N2a neuroblastoma cells also produced appican; however, treatment with dibutyryl cAMP which promotes neuronal differentiation in these cells inhibited its production without inhibiting synthesis of APP. In contrast to the restricted expression of appican, APP was present in all cultures, and its production was independent of appican synthesis. Neuronal cultures produced mainly APP695 while glial cultures produced the Kunitz type protease inhibitor containing APP. The astrocyte-specific expression of appican suggests a function distinct from the function of APP. Brain appicans may play a role in the development of Alzheimer disease neuropathology.
 ...
PMID:The Alzheimer amyloid precursor proteoglycan (appican) is present in brain and is produced by astrocytes but not by neurons in primary neural cultures. 774 33

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.
 ...
PMID:Distribution and characterization of microglia/macrophages in human brain tumors. 887 Aug 31

Neuronal differentiation is well documented in cerebellar primitive neuroectodermal tumors but is uncommon in other cerebellar neoplasms. Although rare, gangliogliomas and gangliocytomas have been previously described in the cerebellum. We report a cerebellar ganglioglioma in a 14-year-old boy, which revealed bizzare markedly pleomorphic cells with extremely pronounced nuclear atypia but less than one mitosis per 50 high-power fields and no necrosis. The tumor showed glial as well as neuronal differentiation, with abundant bi- and multinucleated ganglion cells. There were abundant Rosenthal fibers, eosinophilic granular bodies, focal calcification, and perivascular lymphocytic infiltrates. There has been no evidence of tumor recurrence or neurological deterioration 21 years after surgery, although the marked nuclear atypia led to an initial diagnosis of an anaplastic glioma. We stress the need for careful evaluation of cerebellar gliomas in children that show only nuclear atypia or endothelial hyperplasia in the absence of other features of malignancy.
 ...
PMID:Unusual cerebellar ganglioglioma with marked cytologic atypia. 905 64

Neuronal and glial sodium-dependent transporters are crucial for the control of extracellular glutamate levels in the CNS. The regulation of these transporters is relatively unexplored, but the activity of other transporters is regulated by protein kinase C (PKC)- and phosphatidylinositol 3-kinase (PI3K)-mediated trafficking to and from the cell surface. In the present study the C6 glioma cell line was used as a model system that endogenously expresses the excitatory amino acid carrier 1 (EAAC1) subtype of neuronal glutamate transporter. As previously observed, phorbol 12-myristate 13-acetate (PMA) caused an 80% increase in transporter activity within minutes that cannot be attributed to the synthesis of new transporters. This increase in activity correlated with an increase in cell surface expression of EAAC1 as measured by using a membrane-impermeant biotinylation reagent. Both effects of PMA were blocked by the PKC inhibitor bisindolylmaleimide II (Bis II). The putative PI3K inhibitor, wortmannin, decreased L-[3H]-glutamate uptake activity by >50% within minutes. Wortmannin decreased the Vmax of L-[3H]-glutamate and D-[3H]-aspartate transport, but it did not affect Na+-dependent [3H]-glycine transport. Wortmannin also decreased cell surface expression of EAAC1. Although wortmannin did not block the effects of PMA on activity, it prevented the PMA-induced increase in cell surface expression. This trafficking of EAAC1 also was examined with immunofluorescent confocal microscopy, which supported the biotinylation studies and also revealed a clustering of EAAC1 at cell surface after treatment with PMA. These studies suggest that the trafficking of the neuronal glutamate transporter EAAC1 is regulated by two independent signaling pathways and also may suggest a novel endogenous protective mechanism to limit glutamate-induced excitotoxicity.
 ...
PMID:Multiple signaling pathways regulate cell surface expression and activity of the excitatory amino acid carrier 1 subtype of Glu transporter in C6 glioma. 950 8

Neuronal and mixed glioneuronal tumors traditionally have comprised a very small percentage of intrinsic central nervous system neoplasms, although they are somewhat more common among juvenile brain tumors and in the temporal lobe. Neuronal differentiation increasingly is recognized in pleomorphic xanthoastrocytoma, intraventricular neurocytoma, and subependymal giant cell astrocytoma. However, the diagnostic distinctions between subtle ganglioglioma (with rare neurons) and infiltrating glioma with entrapped neurons and between infiltrating oligodendroglioma and parenchymal neurocytoma are problematic but may be clinically important. Recently, it was proposed that perisomatic synaptophysin immunostaining in the human central nervous system reliably and selectively discriminates neoplastic from nonneoplastic neurons. Using this criterion, the number of brain stem and spinal cord gangliogliomas could be increased substantially. We canvassed synaptophysin immunostaining patterns in the normal brain stem, cerebellum, and forebrain, and found that synaptophysin-positive neurons are distributed broadly in the normal human brain. In disturbed neocortical tissue, such as near vascular malformations, synaptophysin-positive neurons and irregular white-matter synaptophysin immunostaining are visualized. Although synaptophysin-positive neurons are found in gangliogliomas and archipelagos of synaptophysin reactivity are found in neurocytomas, these patterns clearly are not pathognomonic for glioneuronal tumors and must be interpreted with caution whenever other histologic or ultrastructural evidence of neuronal differentiation is lacking.
 ...
PMID:Synaptophysin staining in normal brain: importance for diagnosis of ganglioglioma. 959 24

Mutations in the presenilin 1 (PS-1) gene account for most cases of autosomal dominant early-onset familial Alzheimer's disease (AD). In order to elucidate the cellular expression profile of PS-1 we used a novel N-terminal monoclonal antibody against human PS-1. Immunohistochemical staining was observed strongly in senile plaques, and reactive astrocytes of gray and white matter. Neuronal immunoreactivity, however, was found to be only moderate. RT-PCR analysis of PS-1 mRNA revealed expression throughout human development as well as in human glioma cell lines. Altered PS-1 function may contribute to plaque formation in AD.
 ...
PMID:Prominent expression of presenilin-1 in senile plaques and reactive astrocytes in Alzheimer's disease brain. 983 64


1 2 3 Next >>