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)

A bioluminescent technique was used to show that murine neuroblastoma (NB) cells or cell-free extracts (H variant) were able to enhance the release of reactive oxygen intermediates (ROI) from peritoneal macrophages in vitro. L-variant NB cells were ineffective. Physiological concentrations of met-enkephalin produced the same effect in vitro but not leu-enkephalin. When both H- and L-variant cells, or their extracts, were incubated together with macrophages, ROI production was not increased. Similar findings were detectable when met- and leu-enkephalin were cultured together with macrophages. In vivo, preliminary studies gave the same results. The concentration rate of met- to leu-enkephalin was higher in H-variant than in L-variant NB cells. We conclude from our results that met-enkephalin can enhance the release of ROI from peritoneal macrophages. The difference in the effects produced by the H and L variants is due to differences in the concentrations of enkephalins released.
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PMID:Enhanced oxygen metabolism of peritoneal macrophages in the presence of murine neuroblastoma cells is partly caused by enkephalins. 317 Jul 21

Several human tumour cell lines were screened for secretion of proenkephalin-derived peptides with an antiserum directed to its N-terminus, Met-enkephalin-Arg6,Phe7 and for proopiomelanocortin-derived peptides with an antiserum to beta-endorphin. The neuroblastoma SK-N-MC cell line secreted Met-enkephalin-Arg6,Phe7-immunoreactive peptides in relatively high amounts into the culture medium, although processing was not complete and there was no evidence for free Met-enkephalin-Arg6,Phe7. Gene expression was confirmed by the presence of proenkephalin mRNA and proenkephalin-derived polypeptides in extracts of the SK-N-MC cells and also in the neuroblastoma SH-SY5Y cell line. In the latter cells, however, the expression was approximately 3 times lower, there was less processing of proenkephalin and no evidence for secretion.
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PMID:Expression of the proenkephalin gene in human neuroblastoma cell lines. 338 40

Five opioid peptides (immunoreactivity) derived from their respective opioid precursors were measured in neuroblastoma-glioma hybrid cells (NG 108CC15; pmol/g protein): heptapeptide (Tyr-Gly-Gly-Phe-Met-Arg-Phe), 13.0 +/- 2.6; alpha-neoendorphin, 6.6 +/- 0.8; dynorphin A, 4.4 +/- 1.5; dynorphin A 1-8, 1.3 +/- 0.29; beta-endorphin, 0.3 +/- 0.13. These peptides originate from preproenkephalin A (heptapeptide), prodynorphin (alpha-neonedorphin, dynorphin A, dynorphin A 1-8) and proopiomelanocortin (beta-endorphin). The data suggest the expression of all three known opioid precursors in a single hybrid cell line, permitting a simultaneous investigation of the processing of different opioid peptides under identical experimental conditions.
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PMID:Evidence for the expression of peptides derived from three opioid precursors in NG 108CC15 hybrid cells. 356 21

Two cell culture systems were used for studies of neural functions in vitro. A neuronal hybrid cell line (neuroblastoma x glioma hybrid cells) and primary glial-rich cultures of newborn murine brain. The level of cyclic AMP in both systems is regulated by two groups of hormones, those that stimulate and those that inhibit formation of cyclic AMP. Among the inhibitory hormones active on the hybrid cells are opioids. Therefore the cells are being used in the elucidation of action of opioids. The list of stimulating and inhibitory hormones regulating the primary glial-rich cultures includes several peptide hormones such as the gastrointestinal peptides secretin and vasoactive intestinal peptide, the calcaemic hormones parathyrin and calcitonin, adrenocorticotropin and melanotropins, and somatostatin. Noradrenaline (via alpha- and beta-adrenergic receptors) and adenosine (via A1 and A2 receptors) inhibit and stimulate cyclic AMP synthesis in the primary glial-rich cultures. Bradykinin slowly hyperpolarizes the hybrid cells and elicits formation of cyclic GMP. Both responses desensitize rapidly. Substance P increases the permeability of hybrid cells for Na+, as measured by using 14C-guanidinium as substitute for Na+. Hybrid cells actively accumulate taurine, an amino acid that appears to fulfill important functions in the nervous system. The transport of taurine across the plasma membrane is highly specific for and strictly dependent on Na+. The pumped station hypothesis of taurine action in the nervous system views taurine gradient plus taurine carrier as a transport system for the elimination of sodium from neurons during phases of high neuronal activity.
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PMID:Cell culture as models for studying neural functions. 608 74

Binding of [3H]methionine-enkephalin to intact N1E-115 neuroblastoma cells (competing ligand: naloxone) revealed a homogenous population of receptors with a density (Bmax) of 79.0 +/- 6.5 fmol/mg protein (mean SEM, N = 3) and an apparent Kd of 5.33 +/- 1.63 mM. The order of displacement of [3H]met-enkephalin was met-/leu-enkephalin greater than naloxone greater than morphine, suggesting that it is of the delta receptor class. Specific binding was heat-labile, stereospecific and sensitive to Na+. Adding met-enkephalin to intact neuroblastoma caused reductions of both basal and prostaglandin E1-stimulated levels of cyclic AMP (41.4 +/- 4.0% (N = 6) and 45.1 +/- 2.4% (N = 3) of control levels, respectively). Maximum inhibition (naloxone-reversible) was observed as low as 10(-7) M met-enkephalin. Preliminary results suggest that cells grown in cholesterol-supplemented medium show reduced binding of [3H]met-enkephalin.
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PMID:Opiate peptide receptors on intact NIE-115 neuroblastoma: radioligand binding properties, intracellular response, and effects of increasing membrane cholesterol. 609 92

The mouse neuroblastoma N18TG2 has specific, saturable binding sites for human beta-endorphin (beta h-EP). The affinity and number of sites are 1.1 nM and 280,000 per cell, respectively, beta h-EP binding is not inhibited by [Leu]enkephalin or morphine at concentrations up to 0.1 mM; beta h-EP-(6--31) is a potent inhibitor of binding, and camel beta-EP is much less potent. The data suggest the importance of the nonenkephalin segment of the beta h-EP molecule for interaction with the binding site in N18TG2 cells.
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PMID:Human beta-endorphin: specific binding in neuroblastoma N18TG2 cells. 627 87

The potency of a series of synthetic analogs of beta-endorphin in inhibiting binding of [3H2-Tyr27]-beta h-endorphin to either rat brain membranes or neuroblastoma x glioma hybrid cells (NG108-15) has been determined and compared with the previously determined analgesic potency. There is a very good correlation between inhibitory potency in membranes and cells, but the correlation between analgesic potency and inhibitory potency in either membranes or cells is not as good.
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PMID:Beta-Endorphin. Opiate receptor-binding activity of synthetic analogs modified in the enkephalin segment in rat brain membrane and neuroblastoma x glioma hybrid cell. 628 87

This communication reports for the first time specific binding sites in human neuroblastoma cells for human beta-endorphin (beta h-EP). Three cell lines (IMR-32, NMB and Kelly) were investigated and found to bind tritiated beta h-EP with an apparent dissociation constant of 2.2-4.2 nM. Further characterization with camel beta-EP and synthetic analogs indicated that the binding is most likely mediated by the COOH-terminal segments. beta h-EP-(6-31) had significant potency (15-75%) and beta h-EP-(1-27) was without displacing activity. The camel beta-EP has below 1% of the human beta-EP activity.
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PMID:Beta-endorphin: demonstration of binding sites in three human neuroblastoma cell lines specific for the COOH-terminal segment of the human hormone. 632 87

Human beta-endorphin (beta h-EP) binding on neuroblastoma X glioma hybrid NG108-15 cells using tritiated human beta endorphin (3H-beta h-EP) as a primary ligand was found to have a component which was not displacable with [D-Ser2 )-Leu-enkephalin-Thr6 (DSLET). The beta h-EP binding on these cells after saturation of the delta opiate sites with 200 nM DSLET was further characterized with synthetic beta h-EP analogs. The nonopioid binding site appears to recognize beta h-EP-(6-31), beta h-EP-(21-31) and beta h-EP-(28-31). Under these conditions, these COOH-terminal segments fully displace the tritiated beta h-EP. However, beta h-EP-(1-27) does not further displace 3H-beta h-EP in the presence of DSLET. The fact that a combination of DSLET and beta h-EP-(6-31) results in a full displacement of 3H-beta h-EP provides direct evidence for the existence of two binding sites for beta h-EP in NG108-15 cells, one recognizing the NH2-terminal enkephalin sequence and the other the non-opioid COOH-terminal segment.
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PMID:beta-Endorphin: evidence for the existence of opioid and non-opioid binding components for the tritiated human hormone in NG108-15 cells. 633 52

The syndrome of opsoclonus and myoclonus may be the first presenting symptom of neuroblastoma. The disorder is often controlled by treatment with adrenocorticotropic hormone (ACTH). A child with this disorder and treated with ACTH gel had abnormal uptake of 67Ga in both adrenal glands during studies to attempt to detect an occult neuroblastoma. Repeat 67Ga scans proved to be normal once the ACTH was discontinued and the patient was treated with prednisone. It is concluded that ACTH stimulation of normal adrenal tissue was responsible for these abnormal findings.
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PMID:Positive gallium scan in the syndrome of opsoclonus-myoclonus treated with adrenocorticotropic hormone. 633 27


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