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)

Protein kinase inhibitor H-7 and dibutyryl (dB)-cAMP were found to induce neuritic processes in mouse neuroblastoma N18TG2 cells (36). In the present study, morphological differences between the neurites induced by H-7 and those by dB-cAMP were examined using electron microscopy (TEM and SEM) and tubulin immunohistochemistry. It was observed that: 1) The neurites induced by H-7 were relatively thin and frequently had varicosities. On the other hand, the neurites induced by dB-cAMP were thick but they had few varicosities. 2) Centrioles were frequently observed in the cells treated with dB-cAMP but were not encountered in the H-7-treated cells. 3) TEM and tubulin immunohistochemistry revealed that the main shafts of the neurites induced either by H-7 or dB-cAMP were filled with microtubules, but that the varicosities induced by H-7 contained a smaller amount of microtubules. 4) The stability to colchicine was greater in the neurites induced by H-7 than in those by dB-cAMP. From these features of the neurites, it was inferred that neurite outgrowth induced by dB-cAMP is deeply related to the formation of microtubules and that the neurites induced by H-7 were involved in other processes probably including an adhesive property of cell surfaces.
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PMID:Morphology of neurites from N18TG2 cell induced by protein kinase inhibitor H-7 and by cAMP. 165 Nov 49

The regulation of intracellular calcium by cholinergic agonists was investigated in the human neuroblastoma SH-SY5Y, loaded with fura-2. The resting free Ca2+ concentration in this cell line was 199 +/- 14 nM (mean +/- SEM, n = 19). At 1 mM extracellular Ca2+, high concentrations of carbachol and acetylcholine evoked a biphasic change in intracellular Ca2+ concentration, consisting of a transient initial peak followed by a decline to a plateau that was significantly higher than the basal level. Carbachol (0.5 mM) and acetylcholine (10 microM) caused a maximal increase in the intracellular Ca2+ concentration, reaching a peak of 465 +/- 52 (mean +/- SEM, n = 12) and 422 +/- 48 nM (mean +/- SEM, n = 7), respectively, in less than 4 s. This initial calcium transient declined to a plateau of 268 +/- 36 and 240 +/- 27 nM for carbachol and acetylcholine, respectively, in approximately 40 s. The plateau persisted until the agonist was displaced by the addition of antagonist. Atropine, hexahydrosiladifenidol (HHSD), pirenzepine, and methoctramine inhibited the carbachol-evoked initial calcium transient with Ki values of 0.85 +/- 0.05, 8.3 +/- 1.6, 411 +/- 36, and 240 +/- 46 nM (mean +/- SEM, n = 3), respectively, and the acetylcholine-induced initial calcium transient with Ki values of 0.48 +/- 0.18, 13.5 +/- 8.5, 192 +/- 32, and 414 +/- 25 nM (mean +/- SEM of two experiments), respectively, results suggesting that an M3 muscarinic receptor was predominantly mediating these effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The cholinergic regulation of intracellular calcium in the human neuroblastoma, SH-SY5Y. 194 Sep 18

Neuropeptide Y (NPY) was investigated as a possible tumor marker in pediatric patients with tumors of the sympathetic nervous system. Seven patients with neuroblastoma, 3 patients with ganglioneuroblastoma, and 2 with ganglioneuroma, were compared with 12 matched healthy controls and 34 tumor controls. NPY-like immunoreactivity (NPYLI) was analyzed in extracted plasma using a competitive radioimmunoassay. At diagnosis, plasma NPYLI was significantly increased (p less than .001) in the neuroblastoma patients (352 +/- 99 pM; mean +/- SEM) when compared with healthy controls (36 +/- 4 pM) and tumor controls (30 +/- 2 pM). Ganglioneuroblastoma and ganglioneuroma patients had lower levels (57 +/- 8 pM) than neuroblastoma patients but still significantly higher than the controls. In all patients with sympathetic tumors, the NPYLI level was decreased after treatment. Five neuroblastoma patients relapsed; all had increasing NPYLI levels. In 3 of these patients, incresing NPYLI was the first sign of relapse. Plasma NPYLI correlated well to urinary levels of homovanillic acid. NPY in plasma (NPYLI) may be a clinically useful marker of pediatric neuroblastoma for diagnosis and differential diagnosis. NPYLI correlates well with the clinical course and can be the first sign of relapse. Plasma determinations of NPYLI make it possible to monitor rapid alterations of disease.
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PMID:Neuropeptide Y as a marker in pediatric neuroblastoma. 231 29

Murine neuroblastoma cells (clone N1E-115) possess both high- and low-affinity muscarinic receptors. The low-affinity muscarinic receptor, when stimulated, initiates the formation of cyclic GMP by activating the enzyme guanylate cyclase; whereas stimulation of the high-affinity receptor inhibits prostaglanding E1-mediated cyclic AMP formation by inhibiting the enzyme adenylate cyclase. We have reported that lithium ion (Li+) inhibits cyclic GMP formation mediated by the muscarinic receptor agonist, carbachol, in a concentration-dependent manner and that neither ammonium nor sodium ions have such an effect. We extended this study to show that Li+ was an apparently noncompetitive inhibitor of the low-affinity muscarinic receptor with an IC50(+/- SEM) = 13.6 +/- 0.8 mM. In addition, Li+ with a similar IC50 inhibited the cyclic GMP response in intact cells to sodium azide, which is thought to stimulate guanylate cyclase directly. Moreover, though Li+ was found to have a slight inhibitory effect on prostaglandin E1-stimulated cyclic AMP formation (15% inhibition at 10 mM), it had no effect on the function of the high-affinity muscarinic receptor in intact murine neuroblastoma cells.
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PMID:Lithium ions inhibit function of low- but not high-affinity muscarinic receptors of murine neuroblastoma cells (clone N1E-115). 299 50

The effect of adenosine dialdehyde (AD) on in situ tumor growth and host survival was evaluated in the C1300 murine neuroblastoma tumor model prepared by implantation of murine neuroblastoma cells into A/J mice. AD was administered s.c. by one of the following treatment regimens: regimen A, single daily dose for 5 days; regimen B, minipump infusion for 7 days; regimen C, minipump infusion for 14 days; regimen D, minipump infusion for two 7-day periods interspersed by a 7-day drug free interval. AD doses of 1.5 to 2.5 mg/kg/day infused over a 7-day period (regimen B) significantly increased the mean life span of tumor bearing mice from 20.9 +/- 1.2 days (mean +/- 2 SEM) in diluent treated controls to 35.3 +/- 2.1 days in AD treated animals (mean increase +/- 2 SEM: 69 +/- 10%; P less than 0.0001). This treatment regimen also produced a 56 +/- 13% decrease in tumor diameter (P less than 0.0001). Administration of AD for two 7-day infusion periods, interspersed by a 7-day drug free interval (regimen D), increased mean life span 80% (controls, 21.3 +/- 4.4 days; AD treated 38.4 +/- 5.6 days; P less than 0.0005). Hematopoietic toxicity was not observed when doses between 2 and 3 mg/kg/day of AD were infused for 7 days (regimen B). These data suggest that steady state infusions of AD can significantly suppress murine neuroblastoma tumor growth with little systemic toxicity. In contrast, single daily injections of AD were ineffective and toxic to the tumor bearing host.
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PMID:Inhibitory effect of adenosine dialdehyde on in situ murine neuroblastoma growth. 316 45

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

Ultrastructural study of neuroblastoma group tumors including 7 neuroblastomas, 4 ganglioneuroblastomas, and 2 ganglioneuromas was performed by using both TEM and SEM. Tumor cells showed a wide variation comparable to the developmental stages of nerve cells and were classified into four types according to the neuritic process projections; namely apolar, monopolar, bipolar, and multipolar. Neuroblastoma was composed of small cells of apolar, monopolar, and bipolar types with few multipolar cells. Tumor cells ganglioneuroblastoma and ganglioneuroma were multipolar type. SEM observation demonstrated characteristic varicosities in the elongated neuritis processes, and by TEM examination the dilated portions of these varicosities revealed disruption or disappearance of parallel runnings of the microtubules and microfilaments. TEM examination demonstrated presence of Schwann cells in ganglioneuroblastoma and ganglioneuroma, and satellite cells and perineurial cells in ganglioneuroma. The hitherto undescribed cells with caveolar structure which are thought to be a precursor of these stromal elements were disclosed in ganglioneuroblastoma. In order to evaluate the maturation and prognosis of tumors of this group, stromal differentiation seems to be equally important as ganglionic differentiation because both stromal elements and tumor cells have a common origin of neural crest.
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PMID:Transmission and scanning electron microscopic studies on the tumors of neuroblastoma group. 628 64

Results of hypertension screening using the Doppler technique in a group of premature infants following discharge from an intensive care nursery are reported. Systolic blood pressure (BP) was measured at follow-up in 79/99 premature infants who were cared for in the special care nursery over a 9-month period. The mean BP was 99.3 +/- 2.0 (SEM) mm Hg at a mean age of 14.7 +/- 1.3 weeks; mean age corrected for 40 weeks of gestation was 7.4 +/- 1.3 weeks. Seven infants (8.9%) with BP greater than 113 on three separate occasions were identified as hypertensive. Three of these hypertensive infants were found to have a specific etiology requiring treatment: neuroblastoma, coarctation of the aorta, and unilateral ureteropelvic junction obstruction. No difference was found between the hypertensive and normotensive infants for a variety of perinatal and neonatal factors, including the presence or duration of an umbilical arterial catheter. These data suggest that the premature infant may be at risk for the development of hypertension. In the future, neonatal follow-up programs may find hypertension screening a useful part of their evaluation.
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PMID:Hypertension screening in the follow-up of premature infants. 683 59

Interaction of embryonic chick cerebral cells with the astrocytoma (C6) and neuroblastoma (N2a) cells were examined by SEM. When astrocytoma cells were added to the glial monolayer cell substratum the glial substratum was loosened and astrocytoma cells grew into the gaps of the loosened glial substratum. It is believed that the penetrating property of the astrocytoma cells may be related to the invasiveness of the tumour cells. When neuroblastoma (N2a) cells were added to normal glial substratum, no invasion of the glial substratum was observed. Instead, for the first 2 days the tumour cells rested on the glial substratum and sent out numerous fine filopodia (0.1-0.2 micrometers) closely adhered to the surface of the glial cells. On the third day, the groups of glial cells underneath the neuroblastoma cells, which have been covered by filopodia of the tumour cells were rounded and became retracted from the glial substratum. These morphologically altered cells showed features of the tumour cells. It is therefore speculated that neuroblastoma cells have the ability of changing (transforming?) the glial cells probably through their filopodia. When neuroblastoma cells were added to the astrocytoma substratum, there was an initial reaction on both cell types in which lamellipodia were extremely developed. This initial reaction subsided about 24 hours later and the neuroblastoma cells became more flattened, and grew on the astrocytoma substratum. In this case no rounding up of astrocytoma cells was observed. Normal neuronal cells when added to astrocytoma substratum, showed well differentiated neuronal characteristics. This indicates that neuronal differentiation can be maintained by a tumour substratum.
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PMID:Scanning electron microscopic observations on the interaction between normal neuronal and tumour cells in monolayer culture. 730 94

Adrenomedullin is a potent vasodilator peptide that was isolated from human pheochromocytoma. But the presence of adrenomedullin in the brain has not been clarified. We studied the presence of adrenomedullin in the human brain obtained at autopsy from 6 subjects by radioimmunoassay, as well as in the human adrenal glands and tumor tissues of pheochromocytoma, ganglioneuroblastoma and neuroblastoma. Immunoreactive adrenomedullin was detected in every region of human brain examined (0.26-1.4 pmol/g wet weight) with the highest concentrations found in thalamus (1.40 +/- 0.39 pmol/g wet weight, mean +/- SEM) and hypothalamus (1.28 +/- 0.48 pmol/g wet weight). Reverse phase high performance liquid chromatography showed that the immunoreactive adrenomedullin in the human brain was eluted in the position of synthetic human adrenomedullin 1-52. High concentrations of immunoreactive adrenomedullin were found in human adrenal glands (12.6 +/- 1.0 pmol/g wet weight, n = 7), pheochromocytoma (4.5 +/- 1.5 pmol/g wet weight, n = 11), ganglioneuroblastoma (2.0 +/- 1.3 pmol/g wet weight, n = 4) and neuroblastoma (0.55 +/- 0.21 pmol/g wet weight, n = 3). The present study has shown that adrenomedullin is present in the human brain in high concentrations, suggesting that adrenomedullin acts as a neurotransmitter, neuromodulator or neurohormone in man.
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PMID:Adrenomedullin in human brain, adrenal glands and tumor tissues of pheochromocytoma, ganglioneuroblastoma and neuroblastoma. 774 31


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