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)

The monoclonal antibody 217c, raised by Peng et al. [(1982) Science, Wash. 215, 1102-1104] in mice against the rat glioma cell line C6, can be used as a marker for normal Schwann cells. In mixed cultures of Schwann cells and fibroblasts from neonatal rat sciatic nerve, this monoclonal antibody, detected by indirect immunofluorescence, bound to the surface of cells with the same elongated morphology as those that express a previously described surface antigen, rat neural antigen-1 (Ran-1), defined by polyclonal mouse antisera. In these experiments Ran-1 and the antigenic determinant recognized by monoclonal 217c were both found on normal rat Schwann cells and on the rat glial tumor cell lines C6, 33B and 21A and the pheochromocytoma PC12. Neither anti-Ran-1 nor the monoclonal antibody bound to neurons, fibroblasts or glial cells in newborn rat cerebellum cultures, the rat muscle cell line L6, the transformed rat fibroblast cell line Rat 1, the rat brain tumor cell line B28 or the mouse Schwannoma cell line TR6B. Thus the monoclonal 217c behaved as if it were detecting Ran-1 by binding to normal rat Schwann cells and to those tumor cells that have this antigen. Our data show that this monoclonal antibody is a reliable and convenient marker for rat Schwann cells in culture.
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PMID:A monoclonal antibody equivalent to anti-rat neural antigen-1 as a marker for Schwann cells. 406 57

Effects of TI233, a calmodulin antagonist, on transmitter release were studied using a clonal pheochromocytoma cell line (PC12h). TI233, at a concentration of 30 microM, completely suppressed the release of preloaded [3H]NE and [3H]DA. The 50% suppression dose was around 3 microM. TI233 did not inhibit the [3H]NE release evoked by the calcium ionophore A23187. Electrophysiological examinations using a clonal neuroblastoma x glioma hybrid cell line (NG108-15) revealed that TI233 blocked the voltage-sensitive calcium channel of the membrane in the same concentration range. Thus it was suggested that TI233 inhibited transmitter release from neuronal cells by blocking the entry of calcium to the cytoplasm.
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PMID:Inhibition of transmitter release by TI233, a calmodulin antagonist, from clonal neural cells and a presumed site of action. 613 25

Experiments from several different laboratories are reviewed in which clonal neuronal cell lines are being used to study neuronal cellular functions. Primary emphasis is placed on two cell lines, the neuroblastoma X glioma hybrid clone NG108-15 and the pheochromocytoma clone PC12. These particular cell lines are useful because they display many of the properties normally associated with differentiated neurons. The properties which have been studied include: the regulation of adenylate cyclase and the receptors which activate or inhibit its activity, regulation of the cholinergic properties of NG 108-15 and both adrenergic and cholinergic properties of PC12, the response of PC12 to nerve growth factor, and the regulation of synaptogenesis between NG 108-15 cells and cultured muscle. The goal of the review is to not only summarize the information obtained with these two cell lines but also to emphasize the types of research in which clonal cell lines may be most useful in the future.
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PMID:Regulation of presynaptic cellular function. Biochemical studies using clonal neuronal cells. 616 93

In vitro model systems in neurobiology are available to detect and help characterize various intercellular development signals. The presence of such active substances in conditioned medium (CM) from rat C6 glioma cells (2BD clone) was examined using the pheochromocytoma-derived clonal cell lines PC12 and PCG2. Conditioned medium from C6 monolayers induces neurite outgrowth in PC12 cells and extensive alteration in PCG2 cell morphology by 24 h. This ability of CM was found (1) to remain after dialysis and lyophilization, (2) to be modulated by steroid treatment of C6 monolayers (PC12 cells only) and (3) to be distinct from the influence of NGF. Combinations of CM, nerve growth factor (NGF) and dibutyryl cyclic AMP when given together in pairs to PC12 or PCG2 cells revealed facilitation of neurite formation and cell morphology, respectively. These results suggest possible synergistic interaction between the three factors in the neuroglial regulation of neuronal morphological differentiation.
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PMID:Glial-released proteins: III. Influence on neuronal morphological differentiation. 626 4

Increased cellular adhesion has been postulated to be an early event required of neuroblasts undergoing neurite extension during differentiation. Nerve growth factor (NGF) induces neurite extension in a variety of cell types of neural crest origin. In the PC12 rat pheochromocytoma cell line, which has been proposed as a model for precursor cells to sympathetic neurons, NGF and dibutyryl cyclic AMP (dBcAMP) promote both neurite extension and an increased rate of cell-substrate adhesion. Since dBcAMP can substitute for NGF in this enhancement of adhesion rate in the PC12 cell line, cAMP has been suggested as a second messenger for NGF. We have shown that in two nearly diploid adrenergic like human neuroblastoma clones, the KA and SY5Y cell lines, which also extend neurites in response to both NGF and dBcAMP, only NGF enhances cellular adhesion, as defined by an increase in the number of cells cells prelabeled with 35S-methionine which attach to culture dishes at a given time. Incubation with monospecific antibodies directed against murine beta-NGF abolishes the NGF effect on adhesion. The NGF effect on human neuroblastoma is specific insofar as NGF does not facilitate adhesion of two glioma lines. Unlike the results obtained for PC12, in both SY5Y and KA lines, 1 mM dBcAMP decreases the rate of adhesion to levels significantly below those of controls. Adhesiveness of neuroblastoma cells treated with both NGF and dBcAMP is intermediate between that of cells treated with either agent alone. While theophylline mimics the dBcAMP effect, sodium butyrate has no such effect. At 22 degrees C, the effect of NGF on neuroblastoma substrate adhesion is observable within 5 minutes and persists for 2 hours; treatment of the KA line with NGF at 37 degrees C for 24 hours results in a more persistent enhancement of cell adhesion. Furthermore, both SY5Y and KA exhibit different morphologies when challenged with NGF, dBcAMP, or sodium butyrate. This study suggests that NGF and cyclic AMP do not share a common mechanism of action, but can in fact interact antagonistically in an adrenergic like neuroblastoma model system. Furthermore, the results suggest that increased cellular adhesiveness may not be an obligatory prerequisite for neurite extension by neuroblasts in development.
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PMID:Nerve growth factor and cyclic AMP: opposite effects on neuroblastoma-substrate adhesion. 629 16

The precise role of the nerve growth factor protein (NGF) during the growth and development of the human nervous system is not determined. Although it appears to influence a number of neural functions, its mechanism of action is poorly understood. A number of researchers have proposed that NGF may be involved in several pathological conditions including cancer. It has been shown that NGF is secreted by certain sarcoma (23), neuroblastoma (113), and glioma (7,102,136) cell lines and can bind to neuroblastoma and metastatic melanoma cell lines (42). Neuroblastoma (136,181) and pheochromocytoma (165) cells in vitro can be induced by NGF to differentiate toward a morphologically "more benign" state and appropriate NGF treatment of rats can reduce the number of chemically induced gliomas and neurinomas (174,178). NGF can also reduce the growth of intracerebrally inoculated anaplastic glioma cells (172). Anti-NGF treatment of rats (178) and mice (179) can alter the tumor distribution observed following ethylnitrosourea or benzo(a)pyrene treatment (10). In humans, it has been reported that serum levels of NGF are usually elevated in persons "at risk" for neurofibromatosis (156). The precise nature of the NGF role is not known in these instances. Further understanding of the action of NGF could be of clinical importance.
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PMID:Nerve growth factor and neural oncology. 630 Apr 14

An autopsy case of von Recklinghausen's disease (vRD) associated with malignant pheochromocytoma is reported. The patient is a 36-year-old Japanese male and diagnosed as vRD both clinically and pathologically. He died from right adrenal tumor with wide spread metastases to lungs and bone marrow. The tumors presented satisfactory histological features in favor of pheochromocytoma and neurosecretory granules were demonstrated in both primary and metastatic lesions ultrastructurally. Statistical study of 182, 673 autopsy cases from Annuals of Japanese Autopsy Cases was also done in order to investigate the relationship between vRD and associating tumors including benign and malignant pheochromocytoma. Cases with vRD showed significantly higher incidences of malignant Schwannoma, neurofibrosarcoma, intracranial glioma, and pheochromocytoma compared to that of non-vRD cases. Other malignancies revealed rather smaller incidences than non-vRD cases. These neurogenic tumors are to be principal life threatening problems in patients with vRD. Rare incidence of malignant pheochromocytoma in vRD is to become from low incidence of pheochromocytoma, though significantly greater than that of non-vRD cases.
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PMID:Von Recklinghausen's disease (neurofibromatosis) associated with malignant pheochromocytoma. 643 30

Tetrahydrobiopterin content was determined in several clonal cell lines by reversed-phase HPLC and subsequent electrochemical detection. The same chromatography system was used to determine the total biopterin (tetrahydrobiopterin and 7,8-dihydrobiopterin) by fluorescence detection. The catecholamine-producing clones neuroblastoma N1E-115 and pheochromocytoma PC-12 contained 96 and 60 ng tetrahydrobiopterin/mg protein, respectively. The corresponding amount for the neuroblastoma clone N2A was 36 ng/mg protein. The tetrahydrobiopterin content in C-6 glioma cells was below the limit of detection. The total biopterin is about 20% above the tetrahydrobiopterin content. Tetrahydrobiopterin and biopterin from the cells were identified by coelution with standard solutions and by potential-current relationship or emission and excitation spectra, respectively. Addition of 2,4-diamino-6-hydroxypyrimidine, an inhibitor of biopterin synthesis from GTP, to the culture medium of PC-12 cells resulted in a dose-dependent decrease of tetrahydrobiopterin and total biopterin content within 4 h, suggesting that the cells are capable of synthesising the biopterin which was found. A decrease in intracellular tetrahydrobiopterin levels by different concentrations of 2,4-diamino-6-hydroxypyrimidine reduces the cellular production of dihydroxyphenylalanine after inhibition of aromatic L-amino acid decarboxylase, indicating that the concentration of tetrahydrobiopterin might be a limiting factor for catecholamine synthesis in catecholamine-producing cells.
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PMID:Tetrahydrobiopterin and total biopterin content of neuroblastoma (N1E-115, N2A) and pheochromocytoma (PC-12) clones and the dependence of catecholamine synthesis on tetrahydrobiopterin concentration in PC-12 cells. 669 75

A number of neural and nonneural tumor cell lines of rat and human origin were assayed for neuron-specific enolase (NSE) by radioimmunoassay. Most neural tumor cell lines had appreciably higher levels of NSE than did the nonneural tumor cell lines, the highest levels being found in two anaplastic rat glioma lines ( F98 and T24). These two lines contained more than twice the amount of NSE found in a rat pheochromocytoma line (PC12) and in neuroblastoma lines derived from rats ( B35 and B50 ) or humans (IMR-32 and SHSY - 5Y ). Several of the rat glioma and schwannoma lines were inoculated intracerebrally into syngeneic rats. In the resulting tumors, NSE was demonstrable by immunohistochemistry only in those from the F98 and T24 cell lines. A number of ethylnitrosourea-induced rat tumors were also examined immunohistochemically for NSE: NSE was demonstrated in three anaplastic gliomas; three astrocytomas; and two mixed gliomas. Reactive astrocytes were also positive. Fibroadenomas of apocrine and mammary glands in rats were weakly positive, but other extraneural tumors tested were negative. Since normal neuronal elements, axonal swellings, and amine precursor uptake and decarboxylation cells are strongly positive for NSE, whereas glia and most other normal cells are negative, we hypothesize that the elevated metabolic demands imposed on neoplastic and reactive glial cells and on some extraneural tumors necessitate the opening up of metabolic pathways that are normally operative only in neurons and neuroendocrine cells, therefore resulting in the synthesis of the more stable neuron-specific form of enolase.
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PMID:Immunoradiometric and immunohistochemical demonstration of neuron-specific enolase in experimental rat gliomas. 672 96

When the NGF-secreting C-6 rat glioma cells were intracerebrally injected with F98 rat anaplastic glioma cells into rats syngeneic for the F98 cells, an increased mean survival time was observed for rats developing tumors compared with those injected with only anaplastic glioma cells. Thirty percent of the rats injected with both cell types showed no signs of tumor at 90 days. Pretreatment of the anaplastic glioma cells with conditioned medium of C-6 cells did not duplicate these results unless the C-6 cells were pretreated with 17 beta-estradiol, which appears to induce secretion of an adhesion factor as well as NGF. These rats survived even longer and 33% were free of tumors at 90 days. Histological examination of tumors of the nonsurviving rats revealed that they were basically well differentiated with only small anaplastic areas remaining. Both NGF and conditioned medium from C-6 and another NGF-secreting line, S-180 mouse sarcoma, induce process formation in F98 cells and in PC12 pheochromocytoma cells, but the processes that appear following NGF exposure are morphologically different from those induced by conditioned medium. Conditioned -medium-treated cells also have a flatter appearance. In F98 cells, NGF takes longer to induce processes than does conditioned medium. The NGF-induced effects observed in both cells are neutralized by anti-NGF IgG, but those induced by conditioned media are not. Nerve growth factor (NGF) induced increased adhesiveness in F98 rat anaplastic glioma and PC12 rat pheochromocytoma cells. Conditioned media are not. Nerve growth factor induced increased adhesive-and PCuced effects observed in both cells are neutralized by anti-NGF IgG, but those induced by conditioned media are not. Nerve growth factor (NGF) induced increased adhesiveness in F98 rat anaplastic glioma and PC12 rat pheochromocytoma cells. Conditioned media are not. Nerve growth factor induced increased adhesive-and PCuced effects observed in both cells are neutralized by anti-NGF IgG, but those induced by conditioned media are not. Nerve growth factor (NGF) induced increased adhesiveness in F98 rat anaplastic glioma and PC12 rat pheochromocytoma cells. Conditioned media are not. Nerve growth factor induced increased adhesive-and PC12 cells. Anti-NGF IgG did not influence this effect on F98 cells and only partially neutralized the effect on PC12 cells, indicating that other factors may be operative in this system. Conditioned medium collected from C-6 cells pretreated with 17 beta-estradiol induced the highest degree of adhesiveness observed in both F98 and PC12 cells, and this action was unaffected by anti-NGF IgG in either case. Conditioned media from other cell lines, a variety of selected proteins, and dBcAMP did not induce increased adhesiveness. The factor responsible for this effect is nondialyzable, heat-sensitive, and ammonium-sulfate-precipitable, and its secretion appears to be stimulated by 17 beta-estradiol.
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PMID:Effect of nerve growth factor producing cells on anaplastic glioma and pheochromocytoma clones: involvement of other factors. 729 47


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