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 potencies of polyphloretin phosphate, di-4-phloretin phosphate, 4-phloretin phosphate and phloretin to inhibit the stimulation of cAMP accumulation by prostaglandins, isoproterenol and adenosine were studied in 2 clonal cell lines of CNS origin. The sequence of potency to inhibit PGE1 effects was the same in neuroblastoma (N4TG3) and human astrocytoma cells (1321N1): di-4-phloretin phosphate greater than polyphloretin phosphate greater than phloretin greater than 4-phloretin phosphate. The inhibition of PGE1 stimulated cAMP accumulation by the most prostaglandin-specific inhibitor di-4-phloretin phosphate was rapidly established after its addition, fully reversible after a 30 min preincubation period and independent of the presence of calcium. Kinetic studies of the inhibition of PGE1 effects by di-4-phloretin-phosphate suggest a different type of inhibition in 1321N1 and N4TG3 cells.
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PMID:Phosphorylated derivatives of phloretin inhibit cyclic AMP accumulation in neuronal and glial tumor cells in culture. 3 41

The various stages of divergent neuroepithelial differentiation were studied in the solid transplants of a transplantable mouse testicular teratoma (OTT-6050) maintained in both ascitic and solid forms. They included: a) areas of undifferentiated medullary epithelium corresponding to the rare human medulloepithelioma; b) areas of neuroblastic differentiation corresponding to neuroblastoma, with more mature neuronal differentiation corresponding to ganglioneuroma or, when mixed with glial elements, to ganglioglioma; and c) more mature neuroglial areas resembling astrocytoma, oligodendroglioma or ependymoma, as well as more primitive areas corresponding to ependymoblastoma. In tissue culture using collagen-coated coverslips, astrocytic differentiation was found in the outgrowth zone after 15 days, confirmed by immunofluorescence with antibodies to an astroglia-specific protein. In organ culture systems, glial components, including ependymal structures, were preserved in tumor explants, and astrocytic differentiation, as expressed by glial fiber formation, was increased after 4 to 6 weeks in vitro. No neuronal differentiation was demonstrable, however. The neuroepithelial component of this experimental teratoma may provide a model for the study of neoplastic neuroepithelial differentiation.
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PMID:An experimental mouse testicular teratoma as a model for neuroepithelial neoplasia and differentiation. I. Light microscopic and tissue and organ culture observations. 16 76

The regulation of glycogen metabolism in C-6 astrocytoma and C-1300 neuroblastoma cells in culture has been investigated. Two modes of control of glycogen metabolism appear to be operative. The regulation of intracellular glycogen concentrations and the predominant forms of glycogen phosphorylase and glycogen synthase vary with (a) the available energy supply, and (b) altered intracellular concentration of cyclic adenosine 3':5'-monophosphate (cyclic AMP). Both cell lines respond to glucose in the medium; when glucose levels are high, glycogen is synthesized, glycogen phosphorylase a decreases, and glycogen synthase a increases. When glucose in the medium decreases to a critical level, the phosphorylase a increases and glycogen concentrations in the cells decrease in aprallel with the medium glucose. The critical glucose concentration is 2.5 mM for the astrocytoma cells and 4 mM for the neuroblastoma cells. Insulin promotes the conversion of phosphorylase to the b form and synthase to the a form in both cell lines. All of these changes occur without alteration in the intracellular cyclic AMP concentrations. When cyclic AMP concentrations are increased in either cell line, phosphorylase a is increased, synthase a is decreased, and glycogen concentrations decrease. Isobutyl methylxanthine is effective in promoting glycogenolysis in both cell lines. Norepinephrine is effective with the astrocytoma cells, and prostaglandin E1 is effective with the neuroblastoma cells.
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PMID:Regulation of glycogen metabolism in astrocytoma and neuroblastoma cells in culture. 17 53

The effect of the concentration of glucose in the medium on the intracellular concentrations of metabolites of C-6 astrocytoma cells and C-1300 neuroblastoma cells in culture has been investigated. The intracellular concentrations of glucose, glycogen, glucose 6-P and UDP-glucose were measured at intervals after feeding the cells. A rapid increase in glucose and glucose 6-P levels occurred when fresh medium containing 5.5 mM glucose was applied to the cells, followed by slower increases in UDP-glucose andglycogen. When the medium glucose was increased ten-fold, the intracellular concentration of glucose was increased, but the level of glucose 6-P, UDP=-glucose and glycogen were not altered, nor were the rates of accumulation. The addition of insulin to the medium resulted in an increase of intracellular glucose, glucose 6-P and glycogen. The transport of glucose into the cells is not the rate-limiting step of the regulation of metabolite levels in the cells.
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PMID:Glucose transport and metabolism in cultured cells of nervous tissue. 18 38

The effect of sodium n dipropylacetate (nDPA), a competitive GABA-T inhibitor with respect to GABA, has been investigated on glial and neuronal cellular GABA level. After 1 to 4 days incubation with nDPA in the culture medium, a decrease of GABA level in M5 neuroblastoma clonal cell lines and no modification of GABA level in C6 astrocytoma cells has been observed. The combined addition of nDPA 4 micrometer with dibutyryl cyclic AMP (1 mM) to the culture medium induces the same decrease in GABA level in C6 astrocytoma cells as the addition of DB-c-AMP alone. After shorter incubation time with nDPA (5-150 min), we observed a decreased GABA level in C6 astrocytoma glial cells.
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PMID:[Effect of sodium n-dipropylacetate (sodium valproate) on GABA level of neuronal and glial cells in culture]. 21

The case histories of 273 patients with primary neoplasms of the central nervous system seen in The New York Hospital and Memorial Hospital during the years 1968 through 1973 were reviewed. Neoplastic cells were identified in cytologic preparations obtained from 76 patients. These include patients with meningioma, astrocytoma, glioblastoma multiforme, oligodendroglioma, ependymoma, medulloblastoma, neuroblastoma, retinoblastoma, pineoblastoma, and pituitary adenoma. It is concluded that there are certain suggestive cellular features of these neoplasms in cytologic preparations, but additional studies are needed to establish the cytomorphologic characteristics which may aid in the differential diagnosis of primary intracranial neoplasms from extracranial neoplasms which are metastatic to the central nervous system.
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PMID:Cytology of primary neoplasms of the central nervous system. 26 57

Sera from 30 patients with astrocytoma were tested for antibody reacting with cell surface antigens of cultured autologous astrocytoma cells. Ten percent of the patients had antibody detectable by mixed hemadsorption assays, approximately 50% by immune adherence and protein A assays, and 100% by anti-C3-mixed hemadsorption assays. Absorption analysis of reactive sera with autologous, allogeneic, and xenogeneic cells permitted the definition of three classes of astrocytoma cell surface antigens. Class I antigens showed an absolute restriction to autologous astrocytoma cells. Class II antigens were shared by all astrocytomas tested and could be detected also on neuroblastoma, sarcoma, and some (but not all) melanoma cell lines; these antigens were not found on cell lines derived from carcinomas or normal tissues. Class III antigens were widely distributed on cultured normal and malignant cells of human and animal origin. In this series, sera from 2 patients recognized class I antigens, 4 patients' serum recognized class II antigens, and 13 patients' sera recognized class III antigens. Absorption tests have shown that the AJ (class II) antigen of astrocytoma is serologically related to the previously described AH (class II) antigen of melanoma; in tests of nine melanoma cell lines, there was a correspondence between the AJ and AH phenotypes. This method of autologous typing provides a way to classify the cell surface antigens of astrocytomas and to assess the clinical significance of humoral immunity to these antigens.
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PMID:Serological analysis of cell surface antigens of malignant human brain tumors. 28 20

When mouse neuroblasts (clonal line M 1) and hamster astroblasts (clonal line NN) were co-cultured, the originally low activity of acetylcholinesterase of both lines was drastically increased. After 2 months the neuroblastoma M 1 cells were reisolated from the co-culture and were found to contain 10 times higher activity of acetylcholinesterase than the original M 1 cells. This increased activity was maintained over more than 14 subcultures. In contrast, co-cultivation of neuroblastoma M 1 cells with rat astrocytoma cells (clonal line C 6) resulted in a decrease of actylcholinesterase activity compared to either original cell line.
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PMID:[Acetylcholinesterase activity of neuroblastoma and different glial cells in co-culture]. 81 44

The release of 14C-containing compounds from rat cortical slices prelabeled with 14C-adenine consisted largely of adenosine (6-7%), inosine (13-18%), and hypoxanthine (70-74%), with small amounts of nucleotides including cyclic AMP and adenine. This efflux was increased by both ouabain (0.1 mM) and veratridine (0.05 mM), the increment in released radioactivity consisting almost entirely of these three compounds. However, relatively more inosine than adenosine output was evoked by ouabain while the reverse was true with veratridine. Phenytoin partially reversed the effect of both depolarizing agents. After prelabeling, the efflux from astrocytoma cell cultures contained predominantly inosine (74%) and hypoxanthine (23%) with little adenosine. Ouabain increased the release of 14C-adenine derivatives, and this increase was diminished by phenytoin. Preliminary studies with neuroblastoma cell cultures have shown considerable variability in the composition of the effluent, with hypoxanthine the prevalent compound and almost no adenosine. Ouabain enhanced the efflux from these cells, and this effect was apparently reversed by phenytoin.
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PMID:Effects of phenytoin on the release of 14C-adenine derivatives. 89 89

A combination of linoleic and linolenic acids has been shown to be able to partly replace serum in maintaining cell division of neural tumor lines. Addition of essential fatty acids to C-6 rat astrocytoma cells grown in serum-deprived medium increased the rate of cell proliferation and restored morphological appearance. Essential fatty acids also restored the rate of 3H-thymidine uptake by N-18 neuroblastoma cells grown in a serum-deprived medium. In the complete absence of serum, neuroblastoma cells were unable to proliferate despite addition of essential fatty acids. These studies indicate the importance of essential fatty acids in controlling the rate of neural tumor proliferation.
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PMID:Effect of essential fatty acids on proliferation of two neural tumor lines. 117 7


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