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)

Typical markers for neurons but not for astroglia have been identified in cells cultured from a sample of normal adult human temporal lobe, which was removed to gain access to a glioma. Cells were grown in medium containing growth factors, including fibroblast growth factor and nerve growth factor. The cells grew slowly (doubling time, 18 days) and have been carried as far as passage 8 over 10 months. Both immunoblotting and immunocytochemistry with redundant antibodies demonstrated the presence of neurofilaments (NF-H, NF-M, NF-L), but not glial fibrillary acidic protein (GFAP). Neuron-specific enolase (NSE) was also found. Morphologically, the cultures consisted of a pleimorphic population of cells with frequent long processes. Cells demonstrating neuronal rather than astroglial markers can be cultured from normal adult human brain.
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PMID:Presence of typical neuronal markers in serially cultured cells from adult human brain. 140 91

Cultures of fetal rat brain cell aggregates and tumor spheroids from the human glioma cell line GaMG were treated with epidermal growth factor (EGF), fibroblast growth factor (FGF) or isoforms of platelet-derived growth factor (PDGF AA or BB). Radioreceptor binding studies displayed a high binding capacity for EGF and FGF, but not binding of PDGF isoforms in the glioma cells. In serum-free culture, 10 ng/ml of both EGF and FGF caused increased growth and cell shedding in the tumor spheroids, whereas PDGF produced no such effect. Similarly, EGF and FGF stimulated tumor cell migration. EGF increased the proliferation and outgrowth of glial fibrillary acidic protein (GFAP)-positive cells in brain cell aggregates, while PDGF AA and BB both stimulated the outgrowth of oligodendrocyte-like cells which were negative for GFAP and neuron-specific enolase. FGF stimulated GFAP+ as well as GFAP- cell types. In co-culture experiments using brain aggregates and tumor spheroids, both EGF and FGF treatment caused increased tumor cell invasion. PDGF had no effect on the tumor cells, but instead stimulated the proliferation of oligodendrocyte-like cells in the brain aggregates. The present results indicate that growth factors may facilitate glioma growth as well as invasiveness, and cause reactive changes in the surrounding normal tissue.
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PMID:Effects of growth factors on a human glioma cell line during invasion into rat brain aggregates in culture. 152 73

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

We examined the effect of lactic acid on cultured human glioma cell lines expressing glial fibrillary acidic protein (GFAP), vimentin and neuron-specific enolase (NSE). The growth of the cells was inhibited by the lactic acid in a dose-dependent manner. At 56 mM of lactic acid, the surviving cells of the KNS-42-c2 cell line developed slender processes and increasingly formed bizzar giant cells. In an immunofluorescence study of the lactic acid-resistant cells, the GFAP-positive cells prominently decreased in number, while the NSE-positive cells clearly increased. The vimentin was not affected throughout the experiment. After removing lactic acid from the medium, the GFAP-positive cells gradually increased in number. The method of dot immunoassay was useful for quantifying GFAP in cellular extracts. It indicated that the amount of GFAP decreased in the cells cultured with lactate-containing media and increased to the primary values after removing the lactic acid. These results may suggest that the morphological and immunochemical diversities of glioma cells are secondarily affected by cellular microenvironments such as lactic acid.
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PMID:Contrary effect of lactic acid on expression of neuron-specific enolase and glial fibrillary acidic protein in human glioma cells. 232 50

Human cell lines with neuronal and neuroendocrine features were examined for their expression of pp60c-src, the cellular homolog of the transforming gene product pp60v-src of Rous sarcoma virus. Four neuroblastoma (LA-N-5, SH-SY5Y, Paju, and SK-N-MC) and three small-cell lung carcinoma (U-2020, U-1690, and U-1285) cell lines were selected on the basis of their stage of neurocrine differentiation, as determined by the expression of neuron-specific enolase. In an immune complex protein kinase assay, all seven cell lines displayed c-src kinase activity which was considerably higher than that found in nonneurocrine cells (human diploid fibroblasts, glioma, and non-small cell lung carcinoma cell lines). Furthermore, the c-src kinase activity, as determined by autophosphorylation or phosphorylation of an exogenous substrate, enolase, correlated with the stage of neurocrine differentiation. There was an approximately 30-fold difference in c-src kinase autophosphorylation activity between the cell lines representing the highest and lowest stages of neurocrine differentiation. A similar variation was found in the steady-state levels of the c-src protein of these cell lines. Highly differentiated neuroblastoma cells expressed two forms of the src protein. Digestion by Staphylococcus aureus V8 protease did reveal structural diversity in the amino-terminal ends of these c-src molecules. In summary, we found a clear correlation between c-src kinase activity and the stage of neuronal and neuroendocrine differentiation. Thus, the phenotypic similarity between neurons and neuroendocrine cells includes high c-src expression.
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PMID:Expression of c-src in cultured human neuroblastoma and small-cell lung carcinoma cell lines correlates with neurocrine differentiation. 283 Apr 84

The Y-79 human retinoblastoma cell line has been used as a model system for studying differentiation of primitive neuroectodermal cells into either glial-like (glial fibrillary acidic protein positive) or neuron-like (neuron-specific enolase-positive) cells. To determine whether Y-79 retinoblastoma cells express neuronotypic calmodulin-binding proteins, Y-79 cells were either treated with butyrate or dibutyryl cyclic AMP (dbcAMP) in serum-containing medium or were maintained in serum-free media. Using a biotinylated calmodulin blot overlay technique, we found that Y-79 cells treated with dbcAMP or butyrate expressed low levels of membrane-bound calmodulin-binding proteins of 150, 147, 127, and 126 kilodaltons (kDa); butyrate-treated cells also expressed a calmodulin-binding peptide of 135 kDa. Since butyrate treatment of Y-79 cells induces the expression and the secretion of interphotoreceptor retinoid-binding protein (IRBP, 140 kDa), we tested the hypothesis that the calmodulin-binding protein of 135 kDa induced by butyrate treatment was IRBP. Purified bovine IRBP did not bind calmodulin; further, the 135-kDa calmodulin binding protein was not immunoreactive with antisera directed against IRBP. Since dbcAMP and butyrate induce some glial-like characteristics in Y-79 cells, we compared the calmodulin-binding protein pattern in these cells with that seen in human HTB-14 glioma cells. The HTB-14 line did not express calmodulin-binding proteins, even after treatments with agents that induce morphologic change in these cells. Thus, we conclude that Y-79 cells express membrane-bound calmodulin-binding proteins, but in a pattern different from that seen with adult, differentiated neurons or from human HTB-14 glioma cells.
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PMID:Calmodulin-binding proteins in human Y-79 retinoblastoma and HTB-14 glioma cell lines. 283 19

Calmodulin is present in higher concentrations in brain tissues. The content rapidly increased during the 2nd postnatal week in rat brain. Although the protein is ubiquitous in all eukaryotic cells, immunohistochemical studies have revealed that calmodulin is mainly localized in the neurons, exhibiting a similar distribution to that of gamma-type neuron-specific enolase. In the mouse retina, both calmodulin and gamma-enolase were found to be localized in optic nerves, ganglion cells, and inner and outer plexiform layers. The development study showed that gamma-enolase increased in the 2nd postnatal week and that the levels of calmodulin did not significantly change in that stage. In the mouse retina with an inherited retinal dysplasia (C3H), in which all the photoreceptor cells degenerate during the 2nd and 3rd postnatal weeks, calmodulin-specific staining decreased in the residual layers. Calmodulin is also enriched in mammalian testes. In the mouse testis, levels of calmodulin were high in the spermatocytes and in the spermatids, as compared to the level in spermatozoa. This suggests that the large amount of calmodulin in the testis may be associated with miotic divisions and/or spermatogenesis. Immunocytochemical staining of calmodulin in C6 glioma cells and PC12 pheochromocytoma cells showed a high level of calmodulin to be localized on the half spindles between poles and chromosomes in mitotic cells. The protein was also shown to be localized on fibrous structures in the interphase of those cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Calmodulin and neuron: immunohistochemical studies]. 307 1

This paper describes the immunohistochemical staining properties of four monoclonal antibodies (MAbs) (CF, EB, AD, and KB) which had been previously shown to be specific for purified neuron-specific enolase (NSE) by a solid-phase radioimmunoassay. In this study, the authors immunostained a spectrum of normal and neoplastic neuronal, "neuroendocrine," and nonneuronal tissues fixed in formalin and embedded in paraffin. Positivity was generally restricted to normal neuronal structures and neuronal tumors, including adrenal neuroblastoma, ganglioneuroblastoma, olfactory neuroblastoma, pheochromocytoma, carotid body paraganglioma, duodenal gangliocytic paraganglioma, and teratoma with neuroepithelial components. Three staining patterns of the normal or neoplastic neuronal structures were observed: two MAbs (CF and EB) stained predominantly the nerve fibers (axoplasm); one (AD) stained predominantly the cell bodies (perikaryon); and one (KB) stained both the axoplasm and the perikaryon. "Neuroendocrine" tumors such as pulmonary small cell carcinoma, pancreatic islet cell tumor, thyroid medullary carcinoma, and carcinoid tumors from various locations showed a variable staining pattern. Tumor cells undergoing mitotic division were usually positive regardless of type. Normal structures other than neuronal or "neuroendocrine," including normal glial cells, were negative. The authors also studied a range of glial cell tumors with MAbs CF and AD as well as with Dako polyclonal antiserum to NSE. The results showed that CF stained the axonal fibers in the normal white matter surrounding these tumors; it did not stain the tumor cells or the perikarya of neurons in the surrounding normal gray matter. AD stained the glioma cells as well as the perikarya and dendrites of neurons in the surrounding normal gray matter; it did not stain the axonal fibers in the surrounding normal white matter. By contrast, the polyclonal antiserum stained all of these structures. The high degree of staining specificity of the MAbs should prove them to be valuable in immunohistochemical diagnosis of tumors as well as in further understanding the role of NSE in neuronal differentiation.
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PMID:Immunohistochemical characterization of a set of monoclonal antibodies to human neuron-specific enolase. 328 44

For the determination of their possible utility as tumors markers, 2 neural-associated isozymes, neuron-specific enolase [(NSE) EC 4.2.1.11] and creatine kinase BB [(CK-BB) EC 2.7.3.2], were quantitated by radioimmunoassay in human neuroectodermal-derived cell lines, primary brain tumors, and sera and cerebrospinal fluid (CSF) from brain tumor patients. The NSE content of neuroblastoma cell lines was more than sixfold that of the glioma and medulloblastoma lines; the CK-BB content of neuroblastoma and medulloblastoma lines was fourfold to nineteen-fold that of the glioma and other lines. Expression of NSE in neuroblastoma cell lines was not related to time in culture and was cell line specific. NSE in ex vivo medulloblastomas was raised six to ten times that in astrocytomas and gliomas, although no significant differences were noted for the CK-BB content. Serum and CSF NSE levels were markedly raised above control values in 10 of 29 and 6 of 10 cases of astrocytoma, respectively. Raised CK-BB levels in serum (greater than 10 ng/ml) and CSF (greater than 12 ng/ml) were found in 9 of 18 and 2 of 10 patients, respectively. These data suggest that NSE is preferentially expressed by neuroblastoma lines and medulloblastomas and that NSE and CK-BB may have clinical utility as markers for prognosis, diagnosis, and monitoring of response to therapy.
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PMID:Differential expression of neural isozymes by human medulloblastomas and gliomas and neuroectodermal cell lines. 346 6

Ependymoblastoma is considered to be a primitive malignant glioma with ependymal differentiation. This rare tumor occurs in very early life and shows rapid growth and a diffuse infiltration through the leptomeningeal space. The tumor cells are highly immature, with numerous mitoses and multilayered ependymal rosettes. The ependymoblastoma described in this report was found in a 17-year-old girl. In spite of detailed clinical and postmortem examinations, no definite primary site was identified in the neuraxis. The lesion spread predominantly throughout the leptomeningeal space. Histological analysis strongly suggested that this tumor originated from a heterotopic glial nest in the subarachnoid space. The absence of immunohistochemical neural tissue markers, glial fibrillary acidic protein, S-100 protein, neuron-specific enolase, and neurofilaments ruled out neuronal or glial differentiation. The authors were unable to find any previous report of primary leptomeningeal ependymoblastoma.
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PMID:Primary leptomeningeal ependymoblastoma. Case report. 370 47


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