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

Mouse neuroblastoma cells (Clone NIR-115) were grown in serum-free (defined) medium, defined medium supplemented with serum, and control medium to determine whether serum-free medium could substitute for serum-containing medium in our studies of the histamine H1 and muscarinic acetylcholine receptors of these cells. The function of these receptors as determined by measurement of receptor-mediated cyclic [3H]GMP formation was absent in cells grown in serum-free medium and increased as the percentage of serum was increased in the defined medium, but never attained the levels found with control cells. Muscarinic receptor number for cells grown in defined medium was 60% above that found for control cells with no change in the affinity of the receptor for the radioligand (--)[3H]quinuclidinyl benzilate. Guanylate cyclase and acetylcholinesterase activities for cells grown in defined medium were 23 and 66% of those found in control cells, respectively. This marked reduction of guanylate cyclase activity in large part explains the lack of function of these receptors.
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PMID:Lack of function of histamine H1 and muscarinic acetylcholine receptors of mouse neuroblastoma cells grown in serum-free medium. 612 10

The regulation of cyclic adenosine 3':5'-monophosphate (cAMP)-binding protein in N-18 neuroblastoma cells in tissue culture was studied by the covalent incorporation of 8-azido-cyclic adenosine 3':5'-[32P]monophosphate, together with the techniques of sodium dodecyl sulfate:polyacrylamide gel electrophoresis and autoradiography. Greater than 95% of the total cAMP binding activity of N-18 neuroblastoma cells was identified as being regulatory subunits of the type I (RI) and type II (RII) species, with RI being the predominant form of the two (RI:RII = 3:1). The specific activity of RI but not of RII increased 3-fold when cells were grown in medium containing 1% rather than 10% fetal calf serum. Under the same conditions, the specific activity of acetylcholinesterase increased 3- to 5-fold. The increase in RI was inversely related to the serum concentration in the medium and was specific for cells at the stationary phase of growth. An increase in intracellular cAMP, concomitant with the increase in RI, was also observed. Morphological examination of stationary-phase neuroblastoma cells maintained in medium containing 1% fetal calf serum suggested the presence of a high proportion of highly-differentiated cells. It is proposed that the regulatory control of RI cAMP-binding protein by serum may involve modulation of intracellular cAMP and that the expression RI may be used as a biochemical index of differentiation in mouse neuroblastoma cells.
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PMID:Regulation of cyclic adenosine 3':5'-monophosphate-binding protein in N-18 mouse neuroblastoma cells. 625 72

The expression of a adenosine cyclic 3':5'-monophosphate (cAMP)-binding protein, regulatory subunit of the type I cAMP-dependent protein kinase (Rl), and its functional significance in the differentiation of N-18 mouse neuroblastoma cells were examined. 8-Azidoadenosine cyclic 3':5'-[32P]monophosphate, a photoaffinity-labeling analog of cAMP, and high-resolution sodium dodecyl sulfate-polyacrylamide gel electrophoresis were used to identify and quantitate cAMP-binding proteins in cell extracts. The induction of differentiation of N-18 mouse neuroblastoma cells, initiated either by adding dibutyryl adenosine cyclic 3':5'-monophosphate to the growth medium or by culturing cells in medium supplemented with 1% fetal calf serum, led to a 3-fold increase in the amount of 8-azidoadenosine cyclic 3':5'-[32P]monophosphate incorporated into Rl, when assayed in vitro. This increased incorporation was attributable to an increase in the amount of Rl rather than to an increase in the affinity of Rl for 8-azidoadenosine cyclic 4':5'-[32P]monophosphate. The subunit molecular weight, isoelectric point, and immunoreactivity of Rl were found to be identical to that of the regulatory subunit of the type I cAMP-dependent protein kinase purified from bovine skeletal muscle. The increase in Rl was not accompanied by an increase in the cAMP-dependent protein kinase activity. DEAE-cellulose column chromatography confirmed the induction of Rl as a free cAMP-binding protein in the differentiated neuroblastoma cells. The possibility of a growth-dependent regulation of Rl was also examined. Addition of 2% dimethyl sulfoxide to cultures of N-18 mouse neuroblastoma cells inhibited cell growth without increasing the specific activity of Rl. Dimethyl sulfoxide had no effect on neurite outgrowth or acetylcholinesterase activity, two parameters characteristic of differentiated cells. The fact that the induction of Rl coincided with differentiation of the neuroblastoma cells suggests that the expression of Rl may be used as a biochemical index of differentiation in these cells. The presence of a free cAMP-binding protein, not associated with cAMP-dependent protein kinase in neuroblastoma cells, raises important considerations concerning the action of cAMP in the regulation of growth and differentiation.
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PMID:Induction of the regulatory subunit of type I adenosine cyclic 3':5'-monophosphate-dependent protein kinase in differentiated N-18 mouse neuroblastoma cells. 627 81

The possible functions of ornithine decarboxylase (ODC) and polyamines in the differentiation of mouse NB-15 neuroblastoma cells were investigated by examining the changes of these parameters in the differentiating and nondifferentiating NB-15 cells over a 5-day culture period. Differentiation of NB-15 cells was induced by the addition of dibutyryl cyclic AMP and 3-isobutyl-1-methylxanthine (1BMX) to the growth medium and was monitored by neurite outgrowth, increases of acetylcholinesterase (AChE), and RI cAMP-binding protein. Plating of NB-15 cells in fresh serum-containing growth medium was accompanied by rapid growth and a marked increase of ODC activity; this early increase of ODC activity was attenuated, both in duration and in magnitude, in the differentiating cells. The spermidine content of the differentiating neuroblastoma cells was significantly lower than that of the nondifferentiating cells. In the fully differentiated neuroblastoma cells, the ODC activity and spermidine content were lower than that of the undifferentiated cells by approximately 15-fold and five-fold, respectively. Based on these results it is proposed that changes of polyamine metabolism may be of significance in the differentiation of mouse neuroblastoma cells.
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PMID:Changes of ornithine decarboxylase activity and polyamine content upon differentiation of mouse NB-15 neuroblastoma cells. 628 99

(R, S)-alpha-Fluoromethylornithine (alpha-FMO), a catalytic irreversible inhibitor of ornithine decarboxylase (L-ornithine carboxy-lyase, EC 4.1.1.17), induced the differentiation of N2a mouse neuroblastoma cells. The effect of alpha-FMO was concentration dependent; approximately 50% of the cell population exhibited neurite outgrowth in the presence of 1 mM alpha-FMO, while higher concentrations caused severe growth inhibition and cell death. The effect of 1 mM alpha-FMO on neuroblastoma differentiation was potentiated greatly by 0.1 to 0.2 mM N6,O2'-dibutyryl adenosine cyclic 3':5'-monophosphate (Bt2cAMP) causing more than 90% of the cell population to differentiate morphologically with thick and long processes; 0.1 to 0.2 mM Bt2cAMP, by itself, had no effect on cell growth and did not induce neurite outgrowth. The effect of alpha-FMO, either by itself or in combination with 0.1 to 0.2 mM Bt2cAMP, on the morphological differentiation of mouse neuroblastoma cells was reversed by the addition of exogenous putrescine or spermidine. The morphological differentiation of mouse neuroblastoma cells induced by 1 mM alpha-FMO plus 0.2 mM Bt2cAMP was accompanied by increases of the regulatory subunit of the type I cAMP-binding protein and acetylcholinesterase activity. These results indicate that the modulation of cellular polyamine contents may be important in neuroblastoma cell differentiation.
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PMID:Effects of inhibitors of ornithine decarboxylase on the differentiation of mouse neuroblastoma cells. 630 69

The ability of retinoic acid (RA) to modulate acetylcholinesterase (AChE) activity in a human neuroblastoma cell line (LN-N-5) was examined. The specific activity of AChE was significantly increased 3 days after exposure of LA-N-5 to RA and reached its maximum values after 9 or more days of culturing. Dose-response experiments demonstrated that large increases of AChE occurred at RA concentrations between 10(-7) and 10(-6) M with maximum AChE values detected at 10(-6)-10(-5) M. Increased AChE activity paralleled neurite outgrowth in LA-N-5 cultures. These findings demonstrate that RA can regulate specific AChE activity in human neuroblastoma cells in a manner consistent with neuronal maturation.
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PMID:Regulation of acetylcholinesterase activity by retinoic acid in a human neuroblastoma cell line. 638 96

Mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, stimulated outgrowth of neurites and increased acetylcholinesterase activity in C1300-N2A murine neuroblastoma cells cultured in medium containing 10% fetal calf serum. Changes in cell morphology and enzyme activity were concentration-dependent in the range of 0.25-25 microM mevinolin, and were accompanied by decreased incorporation of [3H]thymidine into DNA. The expression of differentiated characteristics induced by 25 microM mevinolin was blocked by simultaneous addition of 100 microM mevalonate to the culture medium. The data suggest that changes in intracellular levels of mevalonate or one of its isoprenoid derivatives may play a role in the regulation of cell differentiation.
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PMID:Induction of differentiation in murine neuroblastoma cells by mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase. 656 16

The presence of acetylcholinesterase in the tumour cells of neuroblastoma has been shown by enzyme histochemistry. For comparison, some other tumours likely to be found in children and commonly presenting histologically as small cell tumours have also been studied. Acetylcholinesterase activity was seen in rhabdomyosarcoma, but, compared with neuroblastoma, the activity was focal and sparse. One Ewing's tumour and a lymphoblastic lymphoma were negative for the enzyme reaction. Some of the ultrastructural features of neuroblastoma are correlated with the presence of this enzyme. Acetylcholinesterase enzyme histochemistry may provide a useful adjunct in the distinction of neuroblastoma from other small cell tumours.
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PMID:Histochemical demonstration of acetylcholinesterase in neuroblastoma. 669 92

We have used the method of heavy isotope labeling to study the metabolic turnover of acetylcholinesterase forms in the neuroblastoma-derived T 28 hybrid cells in their differentiated state. These cells contain mostly G1 and G4 forms, together with a small proportion of G2, and secrete all these forms into the culture medium. The cells maintained constant and equal levels of acetylcholinesterase, with the same proportions of molecular forms, in a medium containing heavy isotope-labeled amino acids and in a control light medium of similar composition. In addition, they secreted acetylcholinesterase at the same rate in both media. After transfer of the cells into the heavy medium, heavy isotope-labeled acetylcholinesterase molecules progressively replace preexisting light molecules. We analyzed heavy and light components of acetylcholinesterase for each of the two major G1 and G4 forms, by reconstructing the pattern obtained in sucrose gradient differential sedimentation, using combinations of weighted elementary distributions. Heavy molecules were detected in cellular extracts after about 30 min for G1 and 3 h for G4. Both heavy forms also appeared in the medium after a lag of about 3 h. The cellular complement of G1 was renewed much faster than that of G4, the levels of the light forms being reduced to 50% of the original level after 3.5 and 40 h, respectively. Each of these forms appeared to consist of several metabolic pools, and we present simplified models which describe their possible relationships.
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PMID:Heavy isotope-labeling study of the metabolism of monomeric and tetrameric acetylcholinesterase forms in the murine neuronal-like T 28 hybrid cell line. 670 75

The history of a 6-year-old girl with a tumor originating from thoracic spine and finally becoming resistant to surgery, radio-, and chemotherapy is reported. Tumor-biopsy material was studied by light and electron microscopy, in cell culture, by acetylcholinesterase ultracytochemistry, and by quantitative catecholamine analysis and this led to the rejection of the initial diagnosis of a neuroblastoma. Light microscopy revealed a uniform population of undifferentiated cells incompletely lobulated by broad fibrovascular septa. Using the electron microscope, cells were characterized by large intracellular pools of glycogen, little cytoplasm with an abundance of free ribosomes and a paucity of organelles. A few cells displayed desmosome-like attachment sites. Staining for specific and unspecific acetylcholinesterase was negative with light and electron microscopy, as were the results of catecholamine histofluorescence using the glyoxylic acid method. The latter result was confirmed by the negative outcome of quantitative analyses of dopamine, noradrenaline, and adrenaline with high pressure liquid chromatography nd electrochemical detection in tissue samples. Tumor cells could easily be maintained in culture for up to 4 weeks. None of a variety of treatments that are known to favor expression of neuronal characteristics in neuroblastoma cells (serum withdrawal, nerve growth factor, dbcAMP, dexamethasone) induced morphological differentiation in cultured tumor cells. On the basis of the clinical history, morphology, and of our experiments with tumor cells, the diagnosis of a so-called extraskeletal Ewing's sarcoma is most likely. Our results strengthen the view that a cell biology approach may be valuable in neuroblastoma differential diagnosis.
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PMID:Ultrastructural, biochemical, and cell-culture studies of a presumed extraskeletal Ewing's sarcoma with special reference to differential diagnosis from neuroblastoma. 711 92


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