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Query: UMLS:C0027819 (neuroblastoma)
 27,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenosine 3',5'-cyclic monophosphate (cAMP) may be one of the important factors in regulating the expression of many differentiated functions in neuroblastoma cells, but some of these functions can be induced by agents that do not increase the intracellular level of cAMP. An elevation of the intracellular level of guanosine 3',5'-cyclic monophosphate (cGMP) neither induced differentiation nor antagonized the effects of cAMP. Neuroblastoma cells increased the level of cAMP-binding proteins during differentiation, whereas glial cells and L-cells did not. This might have accounted in part for an increase in the intracellular level of cAMP even in the presence of high phosphodiesterase activity in neuroblastoma cells, since the protein-bound with the same proteins, but cAMP had about 10 times higher affinity than did cGMP. cAMP promoted the organization of microtubules and microfilaments necessary for the expression of differentiated phenotypes. The extension of neurites required the synthesis of new protein, but it did not need the synthesis of new RNA. cAMP induced differentiation in neuroblastoma cells by increasing the expression of some genetic information while suppressing the expression of others; e.g., the activities of neural enzymes increased, whereas the synthesis of histone and the phosphorylation of H1-histone markedly decreased in differentiated cells. A hypothesis was offered: An increase in cAMP phosphodiesterase activity as a result of mutation in the regulatory gene for phosphodiesterase in a single, or group of, dividing nerve cell(s) is the primary lesion that leads to malignancy. Based on the concept that selective cytocytoxic drugs should be used with agents that cause differentiation, a new therapeutic approach was suggested for the treatment of neuroblastoma. This involved administration of sodium butyrate followed by L-DOPA or prostaglandin E1 in the presence of cAMP phosphodiesterase inhibitor followed by the less immunosuppressive vincristine and 5-(3,3-dimethyl-1-triazeno)imidazole-4-carboxamide.
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PMID:Cyclic nucleotides in the regulation of expression of differentiated functions in neuroblastoma cells. 1 Apr 49

A case of meningeal carcinomatosis associated with cerebral metastases from an adrenal neuroblastoma is described. The clinical picture was ushered-in by bilateral sciatic pain in a 50 years old female and was followed by rapidly progressive sensory-motor deficits of the arms and legs, leading to flaccid quadriplegia associated with paralysis of cranial nerves and episodes of mental confusion. Death occurred 4 months alter, in cardiac failure. At autopsy, a bilateral tumor of the adrenal glands was found. No metastases were detected anywhere except in the central nervous system. Histology identified the tumor as a neuroblastoma; meningeal carcinomatosis, radicular infiltration by tumor cells and parenchimal metastases were found in the central nervous system. Neuroblastoma is typically a tumor of childhood, only 13% of them being found in adult's according to Russell and Rubinstein. Meningeal metastases from adrenal neuroblastoma have not hitherto been reported in the literature. In our opinion, the most likely mode of spread of tumor cells to the central nervous system was hematogenous because of the presence of small multiple intraparenchimal metastases; however, possible spread through the perineural lymphatics, as proposed by others, cannot be excluded, due to the prominent localization of tumor cells at spinal roots level. The main differential diagnostic problems (paraneoplastic neuropathy (Wyburn-Mason) and infectious subacute or chronic meningitis) are discussed. The authors stress the emportance of complete cerebro-spinal fluid examination including a careful search for tumor cells.
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PMID:[Meningeal carcinomatosis: clinical and anatomical study of a case of suprarenal neuroblastoma (author's transl)]. 6

Neuroblastoma, which is primarily an extracranial disease, has remote manifestations which can be confusing. Neurologic signs and symptoms such as opsoclonus (dancing eyes), ataxia, blindness, and cord paralysis may precede by several months the manifestations of the primary tumor in a distant site such as the abdomen. Descriptions of nine cases demonstrate the various modes of presentation and some of the unusual aspects of this disease. The recent advent of computed tomography requires a reevaluation of the neuroradiologic approach to the evaluation of neuroblastoma.
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PMID:Remote effects of neuroblastoma. 9 12

Ecto-ATPase and ecto-5'-nucleotidase activities of hamster astroblasts, clonal line NN, and mouse neuroblasts, clonal line Ml in coculture, have been studied. The originally low ecto-ATPase activity in both cell lines increased many fold when these cell lines were cocultured. An increase of ecto-ATPase activity was also found in coculture of neuroblastoma cells with chick fibroblasts. Neuroblastoma Ml cells were separated from coculture with hamster astroblasts after 7 days and 2 months. Reisolated M1 cell lines exhibited higher ecto-ATPase activity than the original M1 cell line. The M1 cell line separated after 2 months of coculture had higher ecto-ATPase activity than the M1 cell line separated after 7 days of coculture with hamster astroblasts. This higher ecto-ATPase activity continued for more than 20 replications after separation of the M1 cells from the glial cells.
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PMID:Neuroblasts-glia interaction in tissue culture as evidenced by the study of ectoenzymes. Ecto-ATPase activity of mouse neuroblastoma cells. 13 72

A biological system consisting of a cell membrane enzyme (Na+-K+)-ATPase responded to exposure to a weak A.C. magnetic field. Analysis of Na+ pump activity in normal mouse (A/J) tissue--(a) Kidney cortex and diaphragm after 11 days of exposure to a magnetic field of 55-60 gauss, 60Hz showed a significant reduction as did (b) liver tissue but at day 17 the levels had returned to the control values. Neuroblastoma cells (C1300) transplanted to A/J mice also showed a reduction in the (Na+-K+)-ATPase activity but this persisted at day 17.
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PMID:Weak A.C. magnetic field effects: changes in cell sodium pump activity following whole animal exposure. 15 71

Neuroblastoma x glioma NG108-15 hybrid cells exposed to N6, O2'-dibutyryladenosine 3':5'-cyclic monophosphate for several days release [3H]acetylcholine in response to serotonin, prostaglandin F2alpha, KCl, or veratridine. NG108-15 cells grown in the absence of dibutyrul cyclic AMP do not respond to an excitatory stimulus by releasing [3H]acetylcholine but can be shifted to a responsive state by treatment with dibutyryl cyclic AMP. Thus, the reactions that are required for acetylcholine release can be regulated in NG108-15 cells, thereby regulating the ability of cells to form synapses and the efficiency of synaptic communication.
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PMID:Regulation of acetylcholine release from neuroblastoma x glioma hybrid cells. 20 94

Neuroblastoma x glioma in NG108-15 cells possess opiate, alpha-adrenergic, and muscarinic acetylcholine receptors, which mediate an inhibition of adenylate cyclase. Growth of cells for 12--48 hours in the presence of a receptor--activator gradually results in a compensatory increase in adenylate cyclase activity. Withdrawal of the receptor ligand then results in relatively long-lived increases in adenylate cyclase activity and intracellular cAMP levels. Thus cells grown in the presence of morphine, norepinephrine, or acetylcholine seem to become dependent on the compound to maintain normal cAMP levels.
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PMID:Studies on synapse formation and opiate dependence. 21 60

Neuroblastoma-glioma hybrid cells of line 108CC-5 were found to contain high levels of soluble adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase activity and high levels of two specific cAMP receptor proteins, RI and RII. Treatment of the hybrid cells with dibutyryl cAMP increased the level of RI but did not significantly affect the level either of RII or of cAMP-dependent protein kinase activity. The effect of dibutyryl cAMP could be mimicked by prostaglandin E1 and 3-isobutyl-1-methylxanthine, both of which are known to raise cAMP levels in neuroblastoma-glioma hybrid cells. Both in control as well as in dibutyryl cAMP-treated cells, RII but not RI was associated with cAMP-dependent protein kinase. Several lines of evidence suggest that RI represents the free regulatory subunit of type I cAMP-dependent protein kinase. The presence of this regulatory subunit as free cAMP receptor protein in neuroblastoma-glioma hybrid cells may be of significance with respect to the regulation of growth and differentiation in tumor cells.
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PMID:Presence of free cyclic AMP receptor protein and regulation of its level by cyclic AMP in neuroblastoma-glioma hybrid cells. 22 64

The regulation of cyclic adenosine 3:5-monophosphate (cyclic AMP) phosphodiesterase activity in homogenates of malignant and cyclic AMP-induced "differentiated" neuroblastoma cells was studied. Neuroblastoma cells of at least three mouse and one human clone had both the low (2 to 4 muM) and the high (66 to 106 muM) Km phosphodiesterase. In cyclic AMP-induced differentiated cells the values of Km were decreased, whereas the values of Vmax appeared to be slightly increased. Magnesium and manganese stimulated phosphodiesterase activity. Calcium, zinc, copper, mercury, ethylenediaminetetraacetic acid, and imidazole completely inhibited phosphodiesterase activity in malignant cells, whereas the above agents, except ethylenediaminetetraacetic acid, only partially inhibited enzyme activity in differentiated cells. Ethylenediaminetetraacetic acid completely reduced phosphodiesterase activity in differentiated cells. The pH optimum for phosphodiesterase activity was about 8 in both malignant and differentiated cells. The present studies show that the values of Km and Vmax and the sensitivity of phosphodiesterase activity to divalent ions change in cyclic AMP-induced differentiated neuroblastoma cells, and therefore we propose that the reverse may be true during malignant transformation of nerve cells.
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PMID:Cyclic adenosine 3':5'-monophosphate phosphodiesterase activity in malignant and cyclic adenosine 3':5'-monophosphate-induced "differentiated" neuroblastoma cells. 23 30

Neuroblastoma cells were synchronized by a combined isoleucine plus glutamine starvation. Adenylate cyclase activity [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] was measured under basal conditions and in the presence of dopamine, adenosine and prostaglandin (PG) E1. A clear dissociation occurred between the respective evolution patterns of basal and agonist-stimulated adenylate cyclase activities. The magnitudes of the enzyme response to PGE1, adenosine, and dopamine also exhibited different evolution patterns during the cell cycle. Evolution of adenylate cyclase responsiveness to PGE1 during the cell cycle exhibited striking similarities with the intracellular 3':5'-cyclic AMP changes observed elsewhere. Use of theophylline and fluphenazine as specific inhibitors of adenosine and dopamine, respectively, made it possible to demonstrate that adenosine, dopamine, and PGE1 stimulated adenylate cyclase through independent receptor sites. Furthermore, whatever the stage of the cell cycle, responses to these three agonists were not additive, indicating that the receptors of adenosine, dopamine, and PGE1 control the same adenylate cyclase moieties. The data suggest that adenylate cyclase cell content and enzyme responsiveness to specific agonists can be independently controlled.
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PMID:Adenylate cyclase from synchronized neuroblastoma cells: responsiveness to prostaglandin E1, adenosine, and dopamine during the cell cycle. 26 97


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