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)

To investigate cell-mediated immune responses to central nervous system tumors, we immunohistochemically analyzed 32 operative specimens, including 19 primary tumors, 5 recurrent tumors, and 8 metastases, for the presence of infiltrating T lymphocytes. In 1 patient, an additional sample of normal brain was studied. Using monoclonal antibodies against T lymphocyte surface markers with a peroxidase technique on frozen sections, we determined that a mild lymphocytic response was present in 3 of 7 primary glial tumors, 1 of 4 recurrent glial tumors, and in 3 of 9 primary meningiomas. The predominant subset was Leu 2, or suppressor/cytotoxic. In contrast, 5 of 7 intracranial metastatic tumors and 1 extracranial metastasis showed marked infiltration with an overall Leu 3, or helper/inducer, predominance. The remainder of the specimens, including 1 recurrent meningioma, 3 neurinomas, and the normal brain sample, were free of infiltrates. Permanent sections revealed an overall pattern of lymphocytic infiltration similar to that of frozen sections. Although additional studies such as electron microscopy are required to establish definitively the lymphocytic nature of the infiltrates, these results support the concept of the ability of the body to mount a cell-mediated response against central nervous system tumors and imply a differential response to primary and secondary tumors.
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PMID:Immunohistochemical analysis of infiltrating lymphocytes in central nervous system tumors. 348 16

Methods are described to study cell surface and cytoplasmic antigens of cultured human glioma, fetal brain cells and fibroblasts using flow cytometry. This required harvesting the cultured cells with Versene or mild trypsin treatment and fixation in 4% paraformaldehyde prior to staining for glial fibrillary acidic protein (GFAP) and fibronectin using indirect immunofluorescence. At passage 10, 38% of fetal brain cells [CHII] were GFAP-positive but at passage 14 only 3.5% expressed GFAP. Two glioblastomas and an anaplastic astrocytoma had 38.8%, 6.7% and 81.3% GFAP-positive cells, respectively. Of the 10(4) cells studied, 91.6%, 79.1% and 40.8% were fibronectin-positive for glioblastoma multiforme [12-18], oligodendroglioma [12-10] and fetal brain [CHII] cells, respectively. Two fibroblast lines had 33.5% and 43.1% of the cells expressing fibronectin. The validity of these results was confirmed by staining for GFAP and fibronectin using peroxidase-antiperoxidase and immunofluorescence microscopy. Using low angle forward light scatter to estimate cell size and gating techniques it was found that GFAP-positive CHII and anaplastic astrocytoma cells were generally larger than GFAP-negative cells of the same type. No correlation between cell size and fibronectin expression was found for glioblastoma [12-18] cells. These results demonstrate the validity of the described methods and illustrate some specific applications and the potential value of flow cytometry to neurooncology.
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PMID:Application of flow cytometry to analyses of cultured human glioma and fetal brain cells. 388 48

Using the peroxidase-antiperoxidase (PAP) technique, we examined 35 primary brain tumors for expression of vimentin and GFAP. Both low-grade and high-grade astrocytomas contained vimentin-positive and GFAP-positive cells. Ependymomas also stained for both markers. In gliosarcomas, the glioblastomatous portions stained like astrocytomas, while only vimentin stain was seen in the fibrosarcomatous portions. Medulloblastomas and oligodendrogliomas were negative for both vimentin and GFAP, while meningiomas contained scattered areas of vimentin-positive cells. These results suggest that the expression of vimentin and GFAP is mostly confined to glial-derived tumors, and that vimentin can potentially be a useful marker for distinguishing undifferentiated GFAP-negative glial tumors and mesenchymal tumors from primitive neuroectodermal tumors.
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PMID:Vimentin and glial fibrillary acidic protein in human brain tumors. 388 31

Glial fibrillary acidic protein (GFAP) was purified from human spinal cord and cerebral white matter. GFAP was localized by an immuno-peroxidase method in normal adult and fetal human brains, rat brains, and 152 central nervous system (CNS) tumors. GFAP was found in reactive and normal astrocytes, immature cells of fetal brain at the 18th to 21st gestational weeks, and normal rat astrocytes. This GFAP staining was quite specific for glial tumors, including astrocytomas, glioblastomas, astroblastomas, and ependymomas. GFAP-positive cells were also found in oligodendrogliomas and choroid plexus papillomas, and they were interpreted as being astroglial or ependymal differentiations. Stromal cells in cerebellar hemangioblastomas were negative. However, engulfed astrocytes were found at the periphery of such tumors and often adjacent to the proliferate blood vessels. In meningiomas, neurinomas, metastatic carcinomas, pituitary adenomas and other non-glial tumors, GFAP-positive cells were not identified.
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PMID:The determination of glial fibrillary acidic protein for the diagnosis and histogenetic study of central nervous system tumors: a study of 152 cases. 409 Oct 41

Seven different experimental glioma models were studied to determine their capillary permeability to horseradish peroxidase. The models were the autochthonous ASV-viral model, intracerebral (ic) and (sc) injections of rat 9L and RG-2 tumor cell lines, the sc rat S-69C15 tumor cell line, and human glioblastoma cell lines in nude mice. The ASV-viral model showed an average HRP permeability of 63% of tumor volume, the ic RG-2 tumors were 100% permeable, and the ic 9L tumors were 41% permeable. The permeability of the marginal zone (brain-tumor interface) showed similar variation from group to group. In contrast, all of the sc tumors were 100% permeable regardless of the cell line used to create the tumors. Our results show the variability between these glioma models, and suggest that RG-2 ic gliomas and all sc gliomas should be optimal to assess the tumoricidal effect of drugs, because access to the tumor compartment from the vascular compartment is complete.
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PMID:Comparative permeability of different glioma models to horseradish peroxidase. 617 14

Regulation of cellular content of the endogenous opioid peptides Met5-enkephalin and Leu5-enkephalin was investigated in neuroblastoma X glioma hybrid cells NG108-15 grown in both serum-supplemented and serum-free defined media. Untreated cells and cells induced to differentiate were stained using anti-Met5-enkephalin and anti-Leu5-enkephalin with the peroxidase-antiperoxidase immunocytochemical technique at the light microscopic level. In untreated NG108-15 cells grown in serum-supplemented medium, intense enkephalin-like immunoreactivity was localized in cell bodies and short processes of a select population of cells. The volume fraction of stained untreated cells remained constant throughout the time period investigated. When cells were induced to differentiate with N6,O2'-dibutyryl adenosine 3':5'-cyclic monophosphate (dBcAMP) or 8-bromo cyclic adenosine monophosphate (1.0 mM) treatment for 5 days, staining was found throughout the cytoplasm of perikarya and the extensive processes which were expressed, and the volume fraction of stained cells increased over 2-fold. Receptor-mediated stimulation of adenylate cyclase by prostaglandin E1 (10 microM) for 5 days produced results similar to those with dBcAMP. Pure cultures of differentiated cells with intense staining were obtained by further treatment of cultures, grown in the presence or absence of dBcAMP, with arabinosylcytosine (araC). Untreated, dBcAMP-treated and araC-treated NG108-15 cells grown in defined medium expressed staining patterns and volume fractions of stained cells similar to those grown in serum-supplemented medium; sodium butyrate (1.0 mM), however, increased the volume fraction of stained cells grown in defined medium over 3-fold, whereas it had little effect on staining of cells grown with serum. The presence of both Met5- and Leu5-enkephalin-like activities in NG108-15 cells was confirmed in acid extracts of cells by radioreceptor assay after separation by reverse phase high pressure liquid chromatography. Induction of differentiation in NG108-15 cells by dBcAMP treatment increased the cellular concentration of both enkephalins to over 2 times the levels found in untreated cells. The biochemical analysis for Met5-enkephalin- and Leu5-enkephalin-like activity compared well with the immunocytochemical data indicating that the enkephalin content is correlated with the state of differentiation of NG108-15 cells.
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PMID:Induction of differentiation increases Met5-enkephalin and Leu5-enkephalin content in NG108-15 hybrid cells: an immunocytochemical and biochemical analysis. 619 53

Immunofluorescence and immunoperoxidase (peroxidase-antiperoxidase, PAP) techniques for the demonstration of neural and non-neural cell markers are contributing greatly to increase the diagnostic accuracy of difficult tumors of the central nervous system. Well characterized nervous system markers include glial fibrillary acidic (GFA) protein, the three protein subunits of neurofilaments, neuron-specific enolase (NSE), myelin basic protein, and S-100 protein. The most important and reliable of these is GFA protein, which is widely in use for the immunohistochemical diagnosis of tumors of the glioma group. Its many practical applications are reviewed and illustrated. Other neural markers, in particular the specificity of NSE and S-100 protein, need to be critically evaluated. Problems related to the immunohistochemical diagnosis of central neuroepithelial tumors of putative neuroblastic origin remain complex and still need to be resolved. Non-neural markers, such as vimentin, desmin, cytokeratins, Factor VIII, alpha-fetoprotein, human chorionic gonadotropin, and immunoglobulins have well defined, although more restricted, applications in surgical neuropathology.
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PMID:Immunohistochemistry of central nervous system tumors. Its contributions to neurosurgical diagnosis. 620 56

Thirty-two cases of human central nervous tumor and one experimental glioma were studied in fixed paraffin or epon embedded tissues using the peroxidase-antiperoxidase method. The present study confirms the usefulness of immunohistochemical methods for the diagnostic evaluation of neuro-epithelial neoplasms. The authors also include some prognostic and histogenetic comments about glial tumors.
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PMID:[Detection of glial fibrillary acidic protein in central nervous tumors using an immunohistochemical method. Preliminary study of 33 cases (author's transl)]. 625 99

The sarcomatous components of most glioma-sarcomas are thought to arise from the neoplastic transformation of hyperplastic endothelial and adventitial vascular cells in a preexisting glioblastoma multiforme. The expression of factor VIII/von Willebrand factor (FVIII/vWF), a marker for endothelial cells, and of glial fibrillary acidic protein (GFAP), a marker for glial cells, was examined in 10 glioblastomas and seven mixed glioma-sarcomas using the peroxidase-antiperoxidase immunohistochemical technique. Hyperplasia of small blood vessels was observed in all 10 glioblastomas; in five, the vascular proliferation had resulted in the formation of prominent glomeruloid structures. FVIII/vWF was detected in the endothelial cells in these vascular structures, but not in the adventitial cells. In the mixed glioma-sarcomas. FVIII/vWF was detected only in endothelial cells; there was no staining for FVIII/vWF in the neoplastic mesenchymal cells. The gliomatous components of the mixed tumors stained intensely for GFAP. These observations indicate that both endothelial and nonendothelial cell types contribute to the small vessel hyperplasia in glioblastomas, and that the sarcomatous components of mixed glioma-sarcomas are derived from either non-endothelial cells or endothelial cells that have undergone antigenic loss following transformation.
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PMID:Immunohistochemical detection of factor VIII/von Willebrand factor in hyperplastic endothelial cells in glioblastoma multiforme and mixed glioma-sarcoma. 628 91

We have investigated the antigenic heterogeneity of human glioma cells and its correlation with other parameters of tumor cell heterogeneity (karyotype, 2':3' cyclic nucleotide 3'-phosphohydrolase expression, in vitro morphology) using the established human glioma cell line D-54 MG and eight single-cell-derived clones. The panel of antibodies used included 3 previously described heterologous sera raised against human gliomas and lamb oligodendroglia and 10 monoclonal antibodies with demonstrated reactivity for tumors of neuroectodermal origin, human fetal tissue, or human Thy-1. Antigen expression was determined by cell surface radioimmunoassay and peroxidase-antiperoxidase immunohistology. The use of a monoclonal antibody panel composed of ten reagents of varied specificity resulted in the demonstration of highly variable and complex antigenic patterns on the cell surfaces of cloned subpopulations of the human glioma cell line D-54 MG. Only one antigen, human Thy-1, was present on the parent line and all clones; the remaining nine antigens exhibited a distribution unrelated to other predictive parameters of genotypic or phenotypic heterogeneity such as karyotype, 2':3' cyclic nucleotide 3'-phosphohydrolase expression, or in vitro morphology. With the exception of clones 3 and 4, which shared a common antigen profile but exhibited distinctly different in vitro morphological patterns, the detected antigenic profile of each clone was distinct, with the proportion of expressed antigens ranging from 2 of 10 (clone 2) to 10 of 10 (clone 1). The demonstration of distinct, selectively maintained cell subpopulations within a human glioma cell line has direct implications for immunotherapeutic designs.
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PMID:Demonstration of complex antigenic heterogeneity in a human glioma cell line and eight derived clones by specific monoclonal antibodies. 630 81


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