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

A panel of monoclonal antibodies to neuroblastoma cells, leucocyte common antigen, vimentin and MHC class II antigens (HLA-DR) and a polyclonal antibody to epidermal keratin were used for immunohistochemistry on sections of ethanol fixed and paraffin embedded specimens from 40 undifferentiated small cell tumours and 10 neural crest neoplasms. With the exception of central nervous system neoplasms and two embryonal rhabdomyosarcomas, immunohistochemical examination discriminated between the neural crest neoplasms and the other small cell tumours. Moreover, the staining pattern of neoplastic cells and structures in the neural crest neoplasms obtained with antibodies to neuroblastoma cells seemed, in part, to reflect the degree of tumour differentiation.
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PMID:Immunohistochemical differentiation of neuroblastomas from other small round cell neoplasms of childhood using a panel of mono- and polyclonal antibodies. 359 75

The presence of 1% ethanol in culture medium during heat treatment (40 degrees C for 8 hours and 43 degrees C for 15 minutes) was sufficient to enhance the effect of hyperthermia on murine neuroblastoma cells (NBP2) in culture, on the criteria of growth (number of viable cells per dish) and survival (colony formation). However, the metabolites of ethanol, acetaldehyde, and sodium acetate at concentrations of 0.003% and 0.125% in culture medium, respectively, under the same experimental conditions did not modify the effect of heat (40 degrees C) on these cells. The presence of same concentration of ethanol, acetaldehyde, or sodium acetate for 15 minutes or 8 hours at 37 degrees C did not affect the growth or the survival of NB cells in culture. These results suggest that ethanol itself rather than its metabolites is responsible for the enhancement of heat effect on NB cells. When ethanol and its metabolites were allowed to remain in the culture medium for the entire periods of heat treatment and observation, they also enhanced the effects of heat on NB cells; however, acetaldehyde was more effective.
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PMID:Ethanol. A heat sensitizer on neuroblastoma cells in culture. 394 38

Twenty common toxic chemicals were tested for their ability to inhibit respiratory activity in cultured mouse neuroblastoma C1300 cells, clone 41A3. Pentachlorophenol and hexachlorophene exhibited the properties of uncouplers of oxidative phosphorylation, whereas for KCN, pyridine, 2,5-hexandione, NaAsO2, K2Cr2O7, HgCl2, methylmercury and triethyltin more simple time-courses of inhibition were obtained. Ethanol, methanol, dimethyl sulphoxide, benzidine, nickel acetate, MnCl2, phenol, CoCl2, Na2SeO3 and CdCl2 did not cause any significant changes in respiratory activity. Among the effective compounds, those with well-known neurotoxic properties were the most potent in inhibiting respiration in 41A3 cells.
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PMID:Effects of toxic chemicals on the respiratory activity of cultured mouse neuroblastoma cells. 407 60

The effect of dl-alpha-tocopheryl (vitamin E) succinate in combination with Prostaglandin A2 (PGA2) and sodium butyrate on mouse neuroblastoma cells (NBP2) in culture, according to the criteria of growth inhibition and morphological differentiation (neurite formation), was studied. Results showed that PGA2 and sodium butyrate inhibited the growth of NB cells in a dose-dependent manner. The combined effects of vitamin E succinate with PGA2 or sodium butyrate, according to the criterion of growth inhibition, were additive. Vitamin E succinate by itself did not induce morphological differentiation, but it enhanced PGA2-induced morphological differentiation. Sodium butyrate alone or in combination with vitamin E succinate did not significantly increase the level of morphological differentiation. Sodium succinate and an equal amount of solvent (ethanol) failed to modify the effect of PGA2 or sodium butyrate. This suggests that the effect of vitamin E succinate in modifying the response of PGA2 and sodium butyrate on NB cells is due to the effect of vitamin E rather than to that of succinate.
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PMID:Effects of dl-alpha-tocopheryl succinate in combination with sodium butyrate and cAMP stimulating agent on neuroblastoma cells in culture. 609 78

Cyclic AMP and glucocorticoids appear to have a role in regulating the activity of tyrosine hydroxylase (TH), as well as the expression of "morphological differentiation" in murine neuroblastoma. Monolayer cultures of C-1300 murine neuroblastoma (clone NBP2) were treated with the following compounds in ethanol: dexamethasone, triamcinolone acetonide, hydrocortisone, cortexolone, androstenedione, testosterone, estradiol-17 beta; or with the phosphodiesterase inhibitor Ro20-1724 [4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone]. Treatment with either 200 micrograms/ml Ro20-1724 or 50 micrograms/ml dexamethasone produced significant increases in TH activity compared to alcohol controls (1.44 vs. 0.82 nmol 14CO2/mg protein/hr compared to 0.095). Triamcinolone acetonide or hydrocortisone also produced smaller, but significant, increases in TH activity compared to dexamethasone. When steroid activities were compared at 25 microM concentration and after 60 min of incubation (to maximize TH activity), triamcinolone acetonide was not as effective (62%) as dexamethasone. The relatively inactive glucocorticoid cortexolone produced a slight but significant increase, while the androgens androstenedione and testosterone and the estrogen estradiol-17 beta were without effect.
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PMID:Glucocorticoids increase tyrosine hydroxylase activity in cultured murine neuroblastoma. 611 72

Strain N2a neuroblastoma cells were grown in monolayer and in spinner culture in Coon's modified Hamms F12 medium, or in Dulbecco's modified Eagle Medium with either high (4.5 g/l) or low (1.0 g/l) glucose, and the specific binding of [3H]GABA and [3H]flunitrazepam were determined. GABA binding was highest in monolayer cells grown in low glucose Dulbecco's, and undetectable in monolayer or spinner cells grown in high glucose Dulbecco's. Binding of flunitrazepam was not sensitive to the medium or culture conditions. Flunitrazepam binding suggested the presence of a 'peripheral' benzodiazepine receptor, because: (a) binding was blocked by RO5-4864 but not clonazepam; (b) binding was not enhanced by 0.1 mM GABA or 50 mM Cl-; and (c) the Kd value was approximately 300 nM. Neither ethanol (100 mM) nor pentobarbital (0.2 mM) had any effect on the binding of GABA; flunitrazepam binding was not affected by ethanol but was decreased about 20% by pentobarbital. GABA, muscimol and veratridine did not alter the membrane potential of the cells, as measured by tetraphenylphosphonium accumulation. The data are discussed in terms of separate receptors for GABA and for benzodiazepines which are not incorporated into a GABA--benzodiazepine receptor--chloride ionophore complex.
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PMID:GABA and flunitrazepam binding to neuroblastoma cell membranes--effects of growth conditions, ethanol and pentobarbital. 612 16

The mouse neuroblastoma-rat glioma hybrid cell line NG108-15 was used to study the acute and chronic interaction of ethanol with intact neural cells. In the short term, ethanol inhibited opiate receptor binding, but after long-term exposure the cells exhibited an apparent adaptive increase in the number of opiate binding sites; this was reversible when ethanol was withdrawn. High concentrations of ethanol (200 mM) increased opiate binding after 18 to 24 hours, whereas lower concentrations (25 to 50 mM) produced similar changes after 2 weeks. This model system has potential for exploring the cellular and molecular mechanisms underlying ethanol intoxication, tolerance, and withdrawal.
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PMID:Ethanol modulation of opiate receptors in cultured neural cells. 631 6

The interaction of ethanol with the nervous system produces acute intoxication, tolerance and withdrawal phenomena. Additionally, there are several alcohol-related neurological disorders which develop in alcoholic patients. Current evidence suggests that ethanol produces some of these changes by altering the structure and function of neural membranes. Therefore, neurotransmitter receptors and receptor-dependent molecular events in the nervous system may be highly sensitive to ethanol. The murine neuroblastoma X glioma hybrid cell line NG108-15 was used to study the acute and chronic interactions of ethanol with intact cells. Ethanol acutely inhibited opiate receptor binding, but after chronic exposure the cells exhibited an apparent adaptive increase in the number of opiate binding sites; this was reversible when ethanol was withdrawn. High levels of ethanol (200 mM) increased opiate binding after 18-24 hours; lower concentrations (25-50 mM) produced similar changes after two weeks. This model system has great potential for exploring the cellular and molecular mechanisms which underlie ethanol intoxication, tolerance and withdrawal.
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PMID:Interaction of ethanol with neural cells in culture: a model of intoxication, tolerance and withdrawal. 656 92

The effect of dl-alpha-tocopheryl (vitamin E) succinate in modifying the radiation response of mouse neuroblastoma (NBP2) and mouse fibroblast (L-cells) cells in culture was studied on the criterion of growth inhibition (due to cell death and inhibition of cell division). Results show that vitamin E succinate markedly enhanced the effect of 60CO-gamma-irradiation on NB cells, but it did not significantly modify the effect of irradiation on mouse fibroblasts. Sodium succinate plus ethanol (0.25% final concentration) did not modify the radiation response of NB cells or fibroblasts. Butylated hydroxyanisole, a lipid soluble antioxidant, also enhanced the effect of irradiation on NB cells, indicating that the effect of vitamin E in modifying the radiation response may be mediated, in part, by antioxidation mechanisms.
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PMID:dl-alpha-Tocopheryl succinate enhances the effect of gamma-irradiation on neuroblastoma cells in culture. 669 72

The effect of dexamethasone on tumorigenicity of cultured neuroblastoma and on de novo synthesis of DNA and protein was determined. Within 12 hr dexamethasone caused a dose-dependent inhibition of [3H]-thymidine incorporation into DNA. Incorporation of [3H]-leucine into protein was not affected by dexamethasone. Neurite formation was interrupted by actinomycin D or cycloheximide. Cells treated with dexamethasone before inoculation into A/J mice produced fewer tumors with longer latent periods than controls. About 2.6 times as many neuroblastoma cells treated with 50 micrograms/ml dexamethasone for 4 days were required for tumor development in 50% of recipient animals as compared to controls. Reduced tumorigenicity was dependent upon the length of treatment and the concentration of dexamethasone used. Cortexolone did not mimic the effects of dexamethasone. If, instead of inoculation, cells were replated and grown without dexamethasone, cellular aggregations appeared among the cells cultured in the absence of dexamethasone. By autoradiography, replated cells previously treated with ethanol displayed uniform incorporation of [3H]-thymidine, whereas replated cells from dexamethasone-treated cultures exhibited no incorporation in differentiated cells. However, incorporation was noted among the clusters. We hypothesize that tumors arising after dexamethasone treatment may be due to the presence of an unresponsive subpopulation of cells.
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PMID:Reduced tumorigenicity of cultured neuroblastoma cells after treatment in vitro with dexamethasone. 689 53


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