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

Normal mouse sera contain naturally occurring antibodies that are cytotoxic in the presence of rabbit complement for NB1, a cell line derived from a neuroblastoma adrenal metastasis of a spontaneous ovarian teratoma. The anti-NB1 antibodies can be specifically removed from normal mouse sera by absorption of the sera with homogenized brain tissue of mouse, rat, guinea pig, chicken, and man and by homogenized kidney tissue of mouse and man. The antigen recognized by anti-NB1 naturally occurring autoantibodies, designated mouse brain antigen-2 (MBA-2), is not present on other normal tissues or tumor cell lines tested. MBA-2 is distinct from previously described mouse brain antigens.
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PMID:Interspecies brain antigen detected by naturally occurring mouse anti-brain autoantibody. 4 48

A 29-year-old pregnant woman diagnosed with acute lymphocytic leukemia maintained remission with daily cyclophosphamide and intermittent prednisone treatment. She delivered a male twin with multiple congenital abnormalities who was diagnosed with papillary thyroid cancer at 11 years of age and stage III neuroblastoma at 14 years of age. The female twin was unaffected and has exhibited normal development to date. First trimester exposure to cyclophosphamide has been associated with major malformations. Metabolites of cyclophosphamide have been demonstrated to be teratogens and carcinogens in animals. Differences in placental or fetal hepatic cytochrome P-450 may account for the variability in response between the twins. In addition, disparity between the twins may be the result of differences in metabolite inactivating enzymes present either in fetal liver or placenta. The risk of second malignancies caused by alkylating agents such as cyclophosphamide has been well documented in adults and children but to the best of our knowledge this is the first description of transplacental second cancer.
Teratog Carcinog Mutagen 1993
PMID:Teratogenicity and carcinogenicity in a twin exposed in utero to cyclophosphamide. 810 55

Stable expression of neuronal receptors in cell lines of neural origin is important for studies of neurotransmitter mediated signal transduction. We have achieved this for the first time in three cell lines which are derived from various tissues of neural origin (hippocampus, HN2; chinese hamster brain explant, NCB-20; rat dorsal root ganglion, F-11). Following electroporation assisted transfer of a construct containing the hippocampal serotonin 5-HT1A receptor (5-HT1AR) DNA, one neural cell line, NG-108-15 (murine neuroblastoma x C6 glioma), failed to express the transfected activity, while three others as well as the non-neural CHO (chinese hamster ovary) cells expressed high levels of the receptor. Upon normalization to coexpressed human beta-hexosaminidase B activity, it was found that the human 5-HT1AR, which is normally concentrated in the hippocampus and at a lesser density in the brain, was expressed at the highest level (15.7 x 10(4) receptors/cell) in the HN2 followed by the NCB-20 (8.3 x 10(4) receptors/cell), F-11 (4.4 x 10(4) receptors/cell) and lastly the non-neuronal CHO (4.2 x 10(4) receptors/cell) cells. Ten-twelve days after passage, a striking increase in expression of the receptor was observed only in the cell lines of neural origin. By contrast, there was no appreciable increase in expression of the transfected 5-HT1AR in the non-neural CHO cells over time. This late increase in expression was eliminated in cells which had been maintained in low glucose (1 g/L) for the first two days after passage, thus establishing a vital role of glucose in expression of the transfected 5-HT1AR in cell lines of neural origin. In all cases the 5-HT1AR was negatively coupled to adenylate cyclase, as evidenced by an agonist mediated decrease in prostaglandin E1 stimulated cyclic AMP levels.
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PMID:Heterologous expression of the serotonin 5-HT1A receptor in neural and non-neural cell lines. 847 11

Neurotransmission is dependent on the presence of neuronal receptors at the synapses, and important cell surface molecules such as gangliosides are pivotal in the maintenance of synaptic contacts. To study the interrelationship between these two classes of molecules, we achieved stable expression of the hippocampus- and CNS-localized serotonin 1A receptor (5-HT1A-R) in three 5-HT1A-R-deficient neuronal cell lines and also the control, non-neural CHO cells. A strong passage dependence of 5-HT1A-R expression, as measured by mRNA levels as well as membrane binding to the selective agonist [3H]8-OH-DPAT, was observed only in the HN2 (hippocampal) and NCB-20 (CNS) cells which are derived from tissues of natural occurrence of the 5-HT1A-R. A paradigm of stress was obtained by carrying out continuous culture of cells without feeding. During this time a dramatic increase in 5-HT1A-R mRNA and [3H]8-OH-DPAT binding was observed only in the neuronal cells after confluence and during decreased cell viability (days 10/11). This was not due to differentiation, since deliberate serum deprivation and differentiation of cells did not result in any dramatic increase in 5-HT1A-R expression. Analysis of ganglioside synthesis by pulse labeling of the transfected cells produced striking results. In the dorsal root of the ganglion (DRG) derived F-11 cells which show low but significant levels of complex gangliosides before transfection, the mere presence of the serotonin 1A receptor resulted in a dramatic increase in synthesis of gangliosides comigrating with GM2, GD1a, GD1b, and GT1b (20-fold by densitometry). In contrast, there was only a 2-fold increase in the overall content of complex gangliosides in the presence of the 5-HT1A-R. In the NCB-20 cells which contain only GD1a but no GD1b or GT1b before transfection, a decrease in GD1a synthesis was observed following transfection. Also agonist (8-OH-DPAT) binding to the serotonin 1A receptor in NCB-20 cells produced a 3-fold increase in synthesis of a ganglioside comigrating with GM3. Thus, our neuroblastoma transfectants help demonstrate stress-induced regulation of the 5-HT1A-R, which in turn exerts a strong and cell type-specific control over such essential cell-surface determinants like gangliosides.
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PMID:Cell-specific regulation of the stably expressed serotonin 5-HT1A receptor and altered ganglioside synthesis. 861 34

Extracellular ATP evoked two excitatory responses in hippocampal neuroblastoma cells (HN2). The first, an opening of a receptor-operated non-selective cation channel and the second was a leftward shift in Na+ channel activation. Both ATP (5-1000 microM) and 2',3'-(4-benzoyl)-benzoyl-ATP (Bb-ATP, 50 microM) activated a non-selective cation current reversing near 0 mV and shifted the Na+ activation and inactivation curves to the left. Based on a comparison of a series of agonists and antagonists, the inward current appeared to be partially mediated by activation of a P2X7 receptor, although hybrid channels cannot be ruled out. The shift in Na+ channel gating could be separated from the opening of the cation channel, as application of the P2Y antagonist Reactive Blue-2 and GTP shifted the Na+ current activation to the left but failed to elicit the inward cation current. Both responses to ATP and Bb-ATP were insensitive to block by the P2X antagonist suramin (300 microM) but were prevented by incubation in oxidized ATP (200 microM); a putative P2X7 receptor antagonist. Prior screening of the surface negative charge of the membrane with a high concentration of divalent cations prevented both responses. We suggest that ATP4- activates a P2X receptor and becomes trapped on a site, on or near the Na+ channel. Activation of the P2X receptor leads to the opening of a non-specific cation channel, while the binding of ATP4- leads to a modified charge sensed by the Na+ channel, similar to what occurs in the presence of charged amphiphiles as well as a number of beta-scorpion toxins.
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PMID:ATP modulates Na+ channel gating and induces a non-selective cation current in a neuronal hippocampal cell line. 1140 29

Sulfur mustard and nitrogen mustard (HN2) are reported to produce neurobehavioral and neuropathological changes in animals and humans, but the mechanisms are unknown. We examined the cytotoxic properties of HN2 in cultures of dividing and post-mitotic neurons and astrocytes, which comprise the majority of cells in the central nervous system. Cultures of rat cerebellar astrocytes, post-mitotic granule cell neurons or dividing and terminally differentiated human SY5Y neuroblastoma cell cultures were treated with various concentrations of HN2 for 24 h. After treatment, culture medium was removed, the cell monolayer was incubated for 30 min with calcein-AM (green, live cells) and propidium iodide (red, dead cells) in control medium, the fluorochrome-containing medium was removed and replaced with control medium and cell density and viability were examined by fluorescence and light microscopy. Extensive cell loss (>90%) was observed in rat neuronal and SY5Y neuroblastoma cell cultures treated with 10 microM HN2, whereas cell loss was similar to controls in comparably treated astrocyte cultures. The DNA from HN2-treated cultures of rat neurons and SY5Y neuroblastoma cells was examined by high-performance liquid chromatography with electrochemical detection for the major HN2 DNA adduct N-(2-hydroxyethyl)-N[2-(7-guaninyl)ethyl]methylamine (GMOH). GMOH was detected in rat neuronal (85 fmol microg(-1) DNA) and SY5Y neuroblastoma cell cultures (46 fmol microg(-1) DNA) treated with 10 microM HN2 for 24 h, but was not detected in comparably treated astrocyte cell cultures. These findings are consistent with HN2 preferentially targeting neurons in vivo, possibly through a mechanism involving DNA damage.
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PMID:In vitro neurotoxic and DNA-damaging properties of nitrogen mustard. 1142 41

The link between exposure to environmental mutagens and the development of cancer is well established. Yet there is a paucity of data on the relationship between gene-environment interactions and the mechanisms associated with the somatic mutational events involved with malignant transformation, especially in children. To gain insight into somatic mutational mechanisms in children who develop cancer, we determined the background mutant frequency (Mf) in the hypoxanthine phosphoribosyl transferase (HPRT) reporter gene of peripheral blood lymphocytes from pediatric cancer patients at the time of diagnosis and prior to therapeutic intervention. We studied 23 children with hematologic malignancies and 31 children with solid tumors prior to initial therapeutic intervention. Children with solid tumors, specifically sarcomas, and Hodgkin's disease were significantly older and had elevated HPRT Mfs (6.1 x 10(-6) and 3.7 x 10(-6), respectively) at the time of diagnosis, compared to normal controls (2.3 x 10(-6)) and other pediatric tumor groups including children with acute lymphocytic leukemia and non-Hodgkin's lymphoma (ALL/NHL, 1.7 x 10(-6)), central nervous system tumors (CNS, 3.6 x 10(-6)), and neuroblastoma (1.9 x 10(-6)). Of importance is that the significant differences observed in HPRT Mfs between these groups no longer existed after correcting for the effects of age. These data demonstrate that in children who develop cancer there appears to be no significant increase in background HPRT Mf that would indicate significant exposure to genotoxic chemicals or an underlying DNA repair defect resulting in genomic instability. In addition, these data demonstrate the importance of correcting for the effect of age when comparing the frequency of somatic mutations in children and should provide baseline data for future longitudinal biomonitoring studies on the genetic effects of chemotherapy in children treated for cancer.
Environ Mol Mutagen 2003
PMID:Comparative analysis of HPRT mutant frequency in children with cancer. 1287 12

1. The serotonin(1A) (5-HT(1A)) receptor is an important representative of G-protein coupled family of receptors. It is the most extensively studied among the serotonin receptors, and appears to be involved in various behavioral and cognitive functions. 2. We report here the pharmacological and functional characterization of the human serotonin(1A) receptor stably expressed in HN2 cell line, which is a hybrid cell line between hippocampal cells and mouse neuroblastoma. 3. Our results show that serotonin(1A) receptors in HN2-5-HT(1A)R cells display ligand-binding properties that closely mimic binding properties observed with native receptors. We further demonstrate that the differential discrimination of G-protein coupling by the specific agonist and antagonist, a hallmark of the native receptor, is maintained for the receptor in HN2-5-HT(1A)R cells. Importantly, the serotonin(1A) receptor in HN2-5-HT(1A)R cells shows efficient downstream signalling by reducing cellular cyclic AMP levels. 4. We conclude that serotonin(1A) receptors expressed in HN2-5-HT(1A)R cells represent a useful model system to study serotonin(1A) receptor biology, and is a potential system for solubilization and purification of the receptor in native-like membrane environment.
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PMID:The human serotonin 1A receptor expressed in neuronal cells: toward a native environment for neuronal receptors. 1712 Jan 64

Palytoxin is one of the most complex and biggest molecules known to show extreme acute toxicity. The dinoflagellate Ostreopsis spp., the producer organism of palytoxin, has been shown to be distributed worldwide, thus making palytoxin an emerging toxin. Rat-derived hepatocytes (Clone 9) and BE (2)-M17 human neuroblastoma cells were used to test palytoxin or palytoxin-like compounds by measuring the cell metabolic rate with Alamar Blue. The dose-dependent decrease in viability was specifically inhibited by ouabain in the case of BE (2)-M17 neuroblastoma cells. This is a functional, dynamic and simple test for palytoxins with high sensitivity (as low as 0.2 ng/ml). This method was useful for toxin detection in Ostreopsis extracts and naturally contaminated mussel samples. A comparative study testing toxic mussel extracts by LC (liquid chromatography)-MS/MS (tandem MS), MBA (mouse bioassay), haemolysis neutralization assay and a cytotoxicity test indicated that our method is suitable for the routine determination and monitoring of palytoxins and palytoxin-like compounds.
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PMID:Specific and dynamic detection of palytoxins by in vitro microplate assay with human neuroblastoma cells. 1868 4

L1 retro-elements comprise 17% of the human genome. Approximately 100 copies of these autonomous mobile elements are active in our DNA and can cause mutations, gene disruptions, and genomic instability. Therefore, human cells control the activities of L1 elements, in order to prevent their deleterious effects through different mechanisms. However, some toxic agents increase the retrotransposition activity of L1 elements in somatic cells. In order to identify specific effects of neurotoxic metals on L1 activity in neuronal cells, we studied the effects of mercury and cobalt on L1-retroelement activity by measuring levels of cellular transcription, protein expression, and genomic retrotransposition in a neuroblastoma cell line compared with the effects in three non-neuronal cell lines. Our results show that mercury increased the expression of L1 RNA, the activity of the L1 5'UTR, and L1 retrotransposition exclusively in the neuroblastoma cell line but not in non-neuronal cell lines. However, cobalt increased the expression of L1 RNA in neuroblastoma cells, HeLa cells, and wild-type human fibroblasts, and also increased the activity of the L1 5'UTR as well as the SV40 promoter in HeLa cells but not in neuroblastoma cells. Exposure to cobalt did not result in increased retrotransposition activity in HeLa cells or neuroblastoma cells. We conclude that non-toxic levels of the neurotoxic agent mercury could influence DNA by increasing L1 activities, specifically in neuronal cells, and may make these cells susceptible to neurodegeneration over time.
Mutat Res Genet Toxicol Environ Mutagen 2014 Jan 01
PMID:Mercury specifically induces LINE-1 activity in a human neuroblastoma cell line. 2424 92


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