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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A metastasizing glioma in a 4-year-old boxer bitch is described. Clinical symptoms included ataxia, blindness, and increased cervical pain sensation. The tumor metastasized to an extraordinary extent via the cerebrospinal fluid. Tumor masses surrounded the whole spinal cord including the cauda equina. Histological examination revealed a variable morphology of the glioma. Immunohistochemical investigations showed some tumor cells reacting with antibodies specific to GFAP and S-100 protein. In contrast, NSE, 200 kd NF, vimentin, and desmin could not be demonstrated within tumor cells. The results are discussed in detail.
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PMID:[Metastasizing glioma in a Boxer]. 194 88

Cultured C6 glioma cells were prelabeled with the plant lectin Phaseolus vulgaris leuco-agglutinin (PHAL) and grafted as a cell suspension (10(6) cells in 5.0 microliters) into freshly made cortical implantation pockets in adult host rats. Animals were killed 1-21 days post-implantation (DPI). The brains were removed, dehydrated, embedded in paraffin and sectioned at 8 microns. Paraffin sections were processed for light level immunofluorescent double labeling for PHAL, a marker for graft derived cells, and glial fibrillary acidic protein (GFAP), a specific marker for C6 glioma cells and astrocytes. Cells positive for both PHAL and GFAP were graft-derived C6 cells. By 7 DPI a large mass developed which extended above the surface of the brain and invaded (displacement of host tissue by a cell mass) the host parenchyma. This mass increased in size over the next 14 days. The invading tumor mass contained double labeled cells at all time periods examined. In addition to the invasion process, grafted C6 cells spread through the host parenchyma by migration (movement of single cells). Individual graft-derived C6 (GFAP/PHAL positive) cells migrated into host cortex surrounding the implantation pocket, corpus callosum ventral to the implantation pocket, ipsilateral internal capsule and bilaterally in the habenula.
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PMID:Individual C6 glioma cells migrate in adult rat brain after neural homografting. 195 Jun 56

A human glioma-derived cell line which expresses both the astrocytic markers, glial fibrillary acidic protein (GFAP) and glutamine synthetase (GS) and cell surface gangliosides recognised by the A2B5 monoclonal antibody has been cloned. Two clones are described, which are A2B5-positive and A2B5-negative, respectively. These neoplastic clones may provide a suitable in vitro model with which to assess the significance of surface ganglioside expression in relation to function and lineage of mammalian glia.
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PMID:A2B5 surface ganglioside binding distinguishes between two GFAP-positive clones from a human glioma-derived cell line. 197 73

Gemistocytes are frequently encountered in cases of reactive gliosis as well as in glial tumors. Recently, miniature forms of gemistocytes (minigemistocytes) were recognized as cellular constituents of oligodendrogliomas. Antibodies specific for the intermediate filaments glial fibrillary acidic protein and vimentin are reactive with gemistocytic cells, but do not react specifically with these cells. In a study of 23 glial tumors we found the monoclonal antibody Pm43 selectively reactive with the classical gemistocytes as well as with the minigemistocytes. Nevertheless, at the ultrastructural level a striking difference in the arrangement of the glial filaments between both gemistocytic cell types was found. Immunoelectron microscopy showed that the reactivity for the newly discovered gemistocytic marker Pm43 was confined to identical intermediate filaments. Despite immunohistochemical homology, a clearly different ultrastructure divides classic gemistocytes and minigemistocytes into two subsets.
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PMID:Ultrastructural and immunohistochemical segregation of gemistocytic subsets. 198 75

The clinical, histological, immunohistochemical, and electron microscopic features of a cerebral astroblastoma are reported. The patient is a young woman with a superficial parietal tumor. Macroscopic findings include a well-delineated superficial nodule with a hard central core. Histological study disclosed a predominantly papillary tumor with hyalinized vessels. Tumor cells were scarcely positive with immunohistochemical stain for glial fibrillary acidic protein, extensive and diffusely positive with vimentin and neuron-specific enolase, and intensely positive with S-100 and epithelial membrane antigen in the papillary areas. Ultrastructural study showed abundant intermediate filaments forming bundles in tumoral cytoplasms, membrane junctions, and external laminae when cells were in contact with collagen fibers. Based on immunohistochemical and ultrastructural characteristics, we believe that the filaments seen in tumor cells are mainly vimentin filaments. These peculiar immunohistochemical patterns in a glioma may aid in the histological diagnosis of this rare tumor type.
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PMID:Astroblastoma: electron microscopy and immunohistochemical findings: case report. 199 Apr 78

Antigen expression in a human glioblastoma was investigated by immunochemical methods in the primary tumor, the first and second recurrence, a permanent cell line derived from the first recurrence and in its xenotransplantation tumors. In the primary tumor, GFAP, vimentin, S100, Leu-7 and glioma-associated antigens (GAA) as defined by the monoclonal antibodies (mAbs) MUC 2-39, MUC 8-22 and MUC 2-63 were markedly expressed. In the recurrences, gradual loss of GFAP and Leu-7 could be observed, whereas S100, vimentin and GAA gave similar results to those in the primary tumor. In contrast, fibronectin and collagen IV, which were restricted to the vessel walls in the primary tumor, were represented in sarcomatous areas of the recurrences. In some of these areas, co-expression of glial cell markers was observed. In short-term cell cultures, expression of glia- and glioma-associated antigens as well as fibronectin and collagen IV was comparable to that of the recurrent tumor tissue. In long-term passages, immunoreactivity of GFAP, Leu-7 and S100 decreased, whereas GAA, vimentin and fibronectin increased. Collagen IV positive cells were not visible beyond passage 15. Transplantation tumors were only partly positive for glial cell markers, but revealed strong immunoreactivity for GAA, fibronectin and collagen IV. With these observations we confirm that the phenotypic variability of glioma cells makes it difficult to identify the origin of cells in human glioblastomas from their antigenicity.
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PMID:Antigen variation in a human glioblastoma: from the primary tumor to the second recurrence, permanent cell line and xenotransplantation tumors. 206 11

Contradictory results have been reported claiming either none, partial or almost complete correlation between the complexity of GSL compound profiles and the assumed glial tumor differentiation. Therefore an attempt was made to compare GSL patterns with both the general (final) tumor diagnosis and malignancy grade (WHO) as well as the regional evaluation of the histology and the grading in the tumor tissue pieces directly subjected to biochemical analysis. Regional and general (final) diagnosis did not always correspond, especially when more than one tissue sample of a given tumor was analyzed. Four GSL component patterns were identified by TLC: GSL-type I with gangliosides primarily of the simple Glac-family lacking sulfatide and the more complex Gtri- and Gtet-gangliosides, GSL-type II with ganglioside of the Glac- and Gtri-families, also without sulfatide, and GSL-type III, with more complex gangliosides of the Gtri- and Gtet-families in addition to Glac-gangliosides and sulfatide, similar to the normal brain pattern, and the pattern of normal brain. There was only insufficient correlation between these GSL-type patterns and final diagnoses. However, between regional diagnosis of astrocytoma II and GSL-type III on the one hand and glioblastoma multiforme IV and GSL-type I on the other hand, a coincidence of more than 85% was found. In only 50% the intermediate GSL-type II and glioma III were associated. There was no relation between GFAP or vimentin expression and histology or GSL-type both with regard to final and regional diagnoses. Regional astrocytoma architectures exhibiting GSL-type III were mostly fibrillary, whilst glioblastomas with GSL component pattern I had often a giant cell make up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tissue architecture and glycosphingolipid content in human gliomas II-IV. 206 94

We show that the expression of the gene encoding glial fibrillary acidic protein (GFAP) gene is affected by at least three cis-acting elements. A positive regulatory element that is located between nucleotides -1,631 and -1,479 can confer cell type-specific expression on a heterologous gene. A second regulatory element is located between nucleotides -97 and -80. The third is a negative regulatory element that is located within the first intron of the gene. Deletion of this element activates GFAP expression in HeLa cells, and affects promoter function in glioma cells.
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PMID:Intragenic sequences affect the expression of the gene encoding glial fibrillary acidic protein. 207 10

Glucocorticoid hormones affect gene expression directly at the level of transcription via intracellular receptors that translocate to the nucleus in the presence of steroid. In the brain, two types of high-affinity receptors bind glucocorticoids, the type I, mineralocorticoid receptor and the type II, glucocorticoid receptor (GR). Both receptor types are expressed by many types of neurons. Although binding studies have suggested that glial cells may also express receptors, the expression of these receptors in specific classes of glia has not been studied previously. This immunocytochemical study was undertaken to determine which of the different classes of glial cells express type II GR. Primary cultures of mixed glial cells from rat cerebrum and cerebellum, purified oligodendrocytes and astrocytes, as well as two glial tumor cell lines were screened for the expression of glucocorticoid receptors using a mouse monoclonal antibody directed against rat liver GR (BuGR-2). Glial cell types were identified by morphology and immunoreactivity (IR) with antibodies directed against glial fibrillary acidic protein (GFAP), cyclic nucleotide phosphodiesterase (CNP), or myelin basic protein (MBP). Double immunofluorescence microscopy revealed that all GFAP-IR cells (type 1 and type 2 astrocytes), all CNP- or MBP-IR cells (oligodendrocytes), as well as immature and intermediate cell types expressed GR, although at different levels. C6 glioma and JScl1 Schwannoma cells were observed to express moderate to high levels of GR. Furthermore, cells grown in the absence of glucocorticoids had diffuse GR staining over the cytoplasm, whereas cells grown in the presence of the synthetic glucocorticoid dexamethasone had strong nuclear staining. These results demonstrate that, in vitro, all classes of glial cells express glucocorticoid receptors that can translocate to the nucleus in the presence of hormone. These observations suggest that glial cells are major targets for glucocorticoid-directed control of gene transcription in the nervous system.
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PMID:Type II glucocorticoid receptors are expressed in oligodendrocytes and astrocytes. 209 80

The activation of cellular proto-oncogenes is related to the genesis and progression of neoplasias. Protein growth factors and their cellular receptors have been identified as products of some proto-oncogenes. The role of epidermal growth factor receptor (EGFr) in gliomas is presented. The expression of mRNA for platelet-derived growth factor (PDGF) and PDGF B-type receptor (PDGF-rec-B) in gliomas is analyzed. Gliomas express "in vivo" PDGF.B and PDGF-rec-B mRNAs. PDGF.B mRNA levels correlate with GFAP mRNA and does not correlate with the degree of malignancy. This is in agreement with the hypothesis of an autocrine growth stimulation in gliomas. However some findings seem to indicate that in these tumors the PDGF-rec-B is preferentially expressed by vascular elements. Thus, also a paracrine loop for endothelial cell growth stimulation may be suggested in malignant gliomas.
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PMID:Oncogenes and growth factors in gliomas. 209 94


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