Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of biogenic amines in cultured cells of mouse neuroblastoma C-1300 (clone NB-2a) was suggested by fluorescence-microscope histochemistry. Incubation in media containing L-[(14)C]tyrosine and L-[(14)C]tryptophan for 24 h, followed by high-voltage electrophoresis, radiochromatogram scanning, and scintillation counting, confirmed the presence of [(14)C]dopamine, [(14)C]norepinephrine, [(14)C]epinephrine, [(14)C]serotonin, [(14)C]tyramine, and [(14)C]octopamine. Dopamine, norepinephrine, epinephrine, and serotonin were demonstrated spectrophotofluorometrically in concentrations, expressed as micrograms amine per milligram protein, of 1.19, 0.027, 0.038, and 0.148, respectively, for cells in a stationary growth phase. Fluorescence-microscope histochemistry also suggested the presence of biogenic amines in cultured astrocytoma cells (cell line C6). Spectrophotofluorometric assay of cells in a stationary growth phase demonstrated intracellular dopamine, norepinephrine, epinephrine, and serotonin in concentrations significantly lower than those of neuroblastoma cells.
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PMID:Biogenic amines in cultured neuroblastoma and astrocytoma cells. 437 Sep 24

It has been proposed elsewhere [Meeker, R.B. & Harden, T. K. (1982) Mol. Pharmacol. 22, 310-319] that muscarinic cholinergic receptor-mediated attenuation of cAMP accumulation occurs through activation of phosphodiesterase in 1321N1 human astrocytoma cells. Pertussis toxin, which ADP-ribosylates the guanine nucleotide regulatory protein involved in receptor-mediated inhibition of adenylate cyclase (Ni), has been utilized to further differentiate between the mechanism of cholinergic regulation of cAMP metabolism in 1321N1 cells and the mechanism involving inhibition of adenylate cyclase in other tissues. Muscarinic receptor-mediated regulation of cAMP accumulation in NG108-15 neuroblastoma-glioma cells occurs through inhibition of adenylate cyclase. Pretreatment of these cells with pertussis toxin completely blocked the capacity of carbachol to attenuate cAMP accumulation. In contrast, concentrations of pertussis toxin two to three orders of magnitude higher than those effective in NG108-15 cells had no effect on muscarinic receptor-mediated attentuation of cAMP accumulation in 1321N1 cells. In addition, no effect of pertussis toxin was observed either on the control rate or the carbachol-stimulated rate of cAMP degradation measured directly in intact 1321N1 cells. A 41,000 Mr protein previously proposed to be the alpha subunit of Ni was labeled during incubation of a plasma membrane fraction from 1321N1 cells with [32P]NAD and pertussis toxin. Pertussis toxin is apparently active in 1321N1 cells, since this protein substrate was not labeled in plasma membrane preparations from cells previously incubated with toxin. Functional activity of Ni was demonstrated by the observation that guanosine 5'-[gamma-thio]triphosphate- and GTP-mediated inhibition of forskolin-stimulated adenylate cyclase activity occurred in cell-free preparations from 1321N1 cells. The inhibitory activity of these guanine nucleotides was lost in membrane preparations from pertussis toxin-treated cells. The data suggest that adenylate cyclase is not involved in cholinergic action in 1321N1 cells and, furthermore, Ni is not involved in muscarinic receptor-mediated activation of phosphodiesterase in these cells. Thus, pertussis toxin can be used to differentiate between two mechanisms of cholinergic regulation of cAMP metabolism.
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PMID:Pertussis toxin differentiates between two mechanisms of attenuation of cyclic AMP accumulation by muscarinic cholinergic receptors. 609 Nov 3

This report documents, in seven infants younger than 2 years of age, a previously unrecognized association of a renal embryonal neoplasm (malignant rhabdoid tumor in six patients and a Wilms' tumor in one) with an embryonal primary tumor originating in the central nervous system. The neuroepithelial tumors included three cerebellar medulloblastomas, one pineoblastoma, one primitive neuroepithelial tumor (probably cerebral neuroblastoma), one malignant subependymal giant cell astrocytoma, and one cerebellar medulloepithelioma with divergent glial and neuronal differentiation. There is no evidence that this association is based on the selective neoplastic transformation of embryonal cells of similar histogenetic or cytogenetic origin. The relationship between these dissimilar, embryologically unrelated tumors remains enigmatic.
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PMID:The association of embryonal tumors originating in the kidney and in the brain. A report of seven cases. 609 60

The attenuation of cyclic AMP accumulation occurs by different mechanisms in 1321N1 astrocytoma cells and NG108-15 neuroblastoma X glioma cells. In 1321N1 cells, cholinergic agonists reduce cyclic AMP accumulation through a Ca2+-dependent activation of phosphodiesterase; in NG108-15 cells, muscarinic receptor-mediated effects on cyclic AMP metabolism occur through inhibition of adenylate cyclase. The goal of the current study was to determine whether different pharmacological specificities were expressed by the muscarinic receptor populations of these two cell lines. The affinity of muscarinic receptors for [3H]quinuclidinyl benzilate (6 pM), [3H]N-methylscopolamine (50 pM), and atropine (80 pM) was similar in membrane preparations from each cell line. The affinity of the antagonist, pirenzepine, which has been proposed to be a selective ligand for a muscarinic receptor subtype, was 3-fold higher in competition binding assays carried out with membranes of 1321N1 cells, than with NG108-15 cells. The Hill coefficients of pirenzepine competition curves were not significantly different from unity in both cell lines. This selectivity of pirenzepine was also apparent in studies of the competitive inhibition of carbachol-induced attenuation of cyclic AMP accumulation in intact cells. Differences in the relative affinities of agonists were observed in competition binding analyses carried out with membranes in the presence of GTP and absence of Mg2+. The Ki values of bethanechol and carbachol were 5- and 12-fold lower for receptors of NG108-15 cells than those of 1321N1 cells and the Ki of methacholine was 3.5-fold lower for 1321N1 cells than for NG108-15 cells. The affinities of oxotremorine and arecoline were similar between the two cell lines. These differences in agonist affinities between the two cell lines were much smaller in analyses of muscarinic receptor-mediated effects on cyclic AMP metabolism in intact cells. Taken together, these data suggest that muscarinic receptors of differing pharmacological specificities regulate cyclic AMP metabolism by different mechanisms in 1321N1 and NG108-15 cells.
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PMID:Muscarinic cholinergic receptors of two cell lines that regulate cyclic AMP metabolism by different molecular mechanisms. 609 92

Previous studies have demonstrated that catecholamine responsiveness in a variety of cells can be altered by inhibitors of RNA and protein synthesis. The neuroblastoma-glioma hybrid, NG108-CC15, which lacks catecholamine-stimulated accumulation of cyclic AMP, was investigated to determine if the responsiveness to prostaglandin E1 (PGE1) could be modified by inhibitors of protein synthesis. Cycloheximide in a time-dependent manner potentiated the ability of prostaglandin E1 to stimulate accumulation of intracellular cyclic AMP. However, the alpha-adrenergic inhibition of the prostaglandin response was not affected by cycloheximide. Withdrawal of norepinephrine following a long-term incubation resulted in a potentiation of subsequent PGE1-stimulated cyclic AMP accumulation. Cycloheximide enhanced this norepinephrine withdrawal effect. Our previous studies have shown that cholera toxin induces refractoriness to beta-adrenergic agonists in C6-2B rat astrocytoma cells and that cycloheximide blocked this action of cholera toxin. In an analogous manner cholera toxin caused refractoriness to subsequent prostaglandin-stimulated cyclic AMP production in NG108-CC15 cells, and cycloheximide reduced cholera toxin-induced prostaglandin refractoriness. Thus cycloheximide potentiates the prostaglandin stimulatory effect, has no effect on the ability of alpha-agonists to inhibit the prostaglandin response, increases the stimulatory effect of PGE1 after norepinephrine withdrawal, and reduces cholera toxin-induced PGE1 refractoriness. these observations suggest that PGE1-stimulated cyclic AMP accumulation in NG108-CC15 cells contains components which are regulated by de novo protein synthesis.
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PMID:Cycloheximide potentiation of prostaglandin E1- and cholera toxin-stimulated cyclic AMP accumulation in NG108-CC15 neuroblastoma-glioma hybrid cells. 626 20

The distribution of the glial fibrillary acidic protein (GFAP) was investigated in sections of 131 paraffin-embedded brain neoplasms obtained at surgery or at autopsy. The unlabeled antibody immunoperoxidase (peroxidase-antiperoxidase, PAP) method was used. Equally good results were obtained from 17-year-old material and from recent material derived at surgery or autopsy and fixed with Bouin fluid or phosphate-buffered formalin. The perikaryons and processes of reactive astrocytes showed the most intense stain for GFAP. Positive reaction to antibody against GFAP of varying intensity was demonstrated in astrocytomas of various grades of malignancy (32 of 32), glioblastoma multiforme (10 of 10), subependymal giant cell astrocytoma (1 of 1), ependymoma (2 of 10), subependymoma (4 of 4), and astrocytes in mixed neoplasms (8 of 8). In two neoplasms diagnosed as malignant astrocytomas and in four neoplasms diagnosed as glioblastoma multiforme, GFAP stain was limited to a few neoplastic cells. Usually the stain was more intense over processes than in perikaryons, with the exception of gemistocytic astrocytomas and the giant cells in glioblastoma multiforme, which showed an equally intense stain over perikaryons and processes. The periphery of Rosenthal fibers was intensely positive for GFAP. In astrocytic neoplasms the number of GFAP-positive cells and the intensity of the stain were inversely proportional to the degree of malignancy. In the following neoplasms the reaction for GFAP was negative: oligodendroglioma (3), oligodendroblastoma (1), medulloblastoma (3), medulloepithelioma (1), neuroblastoma (1), pineocytoma (1), typical teratoma of the pineal (1), fibrosarcoma (1), pituitary adenoma (2), craniopharyngioma (1), chordoma (1), chemodectoma of globus jugulare (1), metastatic carcinoma (17), and lymphoma (8). In one of 18 meningiomas, endogenous peroxidase activity was seen in mast cells. All meningiomas studied were negative for GFAP. In one of six neurinomas a positive reaction for GFAP was detected over processes. The authors concluded that the immunostain for GFAP is useful in the diagnoses of astrocytic neoplasms and of mixed gliomas.
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PMID:Immunocytochemical study of the glial fibrillary acidic protein in human neoplasms of the central nervous system. 628 Nov 68

The effects of mitogenic lectins Phytohemagglutinin (PHA), and Concanavalin A (Con A) on the growth rate of cells derived from glial tumors (astrocytoma, ependymoma, glioblastoma, medulloblastoma, and C6 rat glioma), neural crest tumors (neuroblastoma and schwannoma), and meningiomas were studied. The cell lines were of human and animal origin. The specificity of lectin binding to mitogenic receptors was evaluated using complementary monosaccharides. In all glial- and some neural-crest tumor-derived cell lines, there was a lectin concentration-dependent and cell density-dependent, biphasic growth rate response with stimulation at low and inhibition at high lectin concentrations. This response did not depend on the type of glial tumor, species of origin, or passage level in vitro. Although, in meningioma-derived cell lines, lectins did not induce a growth rate response, they caused morphological changes ("whorling"). Lectin stimulation in glial tumor-derived cell lines resembles that occurring in peripheral blood lymphocytes. Lectin-induced mitogenesis may lay the groundwork for the establishment of a model of glial cell proliferation, and that permits the evaluation of cell surface effects, intracellular mechanisms, and epigenetic factors in studies of tumors, neural development, and neuroimmunology.
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PMID:Mitogenic lectin receptors of nervous system tumors. Study of gliomas, neural crest tumors, and meningiomas in vitro using phytohemagglutinin and concanavalin A. 628 95

Seven children with advanced solid tumors (2 rhabdomyosarcomas, 2 Ewing's sarcomas, 1 astrocytoma, 1 T cell lymphoma and 1 neuroblastoma) received high dose chemotherapy and/or radiotherapy followed by autologous bone marrow transplantation. Four patients achieved complete remissions, two had partial remissions, and one was no response. Side effect of autologous bone marrow transplantation was few compared with that of allogeneic bone marrow transplantation in which graft versus host reaction, profound posttransplantation immunodeficiency and interstitial pneumonitis were unavoidable. In this report methods of bone marrow cryopreservation and elimination of tumor cells from harvested bone marrow were also discussed.
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PMID:[Autologous bone marrow transplantation in solid tumors in children]. 634 80

A cell surface component has been identified that is found on cultured rat dorsal root ganglion neurons and Schwann cells and also cultured brain astrocytes and oligodendrocytes. This component was detected with a monoclonal antibody originally generated to the NG108 (N18 mouse neuroblastoma X C6 rat astrocytoma) hybrid cell line. The antibody, designated B2C11, binds to cultured peripheral nervous system cells: intact dorsal root ganglion and trigeminal neurons and cultured dorsal root ganglion and sciatic nerve Schwann cells. The binding of B2C11 to dorsal root ganglion neurons in vivo was confirmed by immunofluorescence analysis of cryostat sections. However, cultured embryonic rat central neurons showed no detectable binding of B2C11. Cultured brain cells containing glial fibrillary acidic protein (astrocytes) and also oligodendrocytes cultured from corpus collosum did bind B2C11 on their surfaces. B2C11 immunoprecipitation of detergent-solubilized membrane proteins from both lactoperoxidase iodinated C6 and PC12 rat pheochromocytoma cells indicated a single band with an apparent molecular weight of 21,000-23,000. Analysis of B2C11 binding to particulate protein preparations from adult rat organs showed highest specific activity in dorsal root ganglia. Other neural tissues had substantial binding. Some nonneural tissues (lung, kidney, and small intestine) expressed significant antigen levels, whereas others (heart, liver, and skeletal muscle) had a B2C11 antigen-specific activity less than 5% of that of dorsal root ganglia. Thus the B2C11 antigen is enriched in neural tissues, where it is found on the surfaces of a unique set of neuronal and glial cells.
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PMID:Detection of a cell surface antigen found on rat peripheral nervous system neurons and multiple glia: astrocytes, oligodendrocytes, and Schwann cells. 638 27

Acetophenetidines, acetamidophenols, phenetidines and aminophenols substituted in o-, m- or p-position inhibit prostaglandin-synthetases originating from C 1300 mouse neuroblastoma cells (clone N2A), rat astrocytoma cells (clone C 6) and rat renal medulla. Desacetylated compounds were more potent inhibitors than their corresponding acetyl derivatives and many o- and m-analogues were more active than p-substituted structures like paracetamol (p-acetamidophenol) or phenacetin (p-acetophenetidine). When twelve o-, m- or p-aminophenolic test compounds were compared to acetylsalicyclic acid and indomethacin, o-, and p-phenetidine and o-aminophenol were as effective as acetylsalicyclic acid. All aminophenol derivatives which inhibited prostaglandin synthesis suppressed cultured nervous cell and kidney cyclo-oxygenases to similar extents. Our results suggest that aminophenolic drugs are not more effective against prostaglandin-synthetases in the CNS than against those in the periphery.
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PMID:Inhibition of prostaglandin synthetases derived from neuronal and glial cells and rat renal medulla by ortho-, meta- and para-substituted aminophenolic compounds. 640 96


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