Search results for "neuroblastoma."

showing 10 items of 238 documents

Risk estimation in localized unresectable single copy MYCN neuroblastoma by the status of chromosomes 1p and 11q

2006

In localized neuroblastoma, the identification of patients requiring intensive treatment is still difficult. We retrospectively analyzed data of 280 single copy MYCN stage 2 and 3 neuroblastoma patients with gross residual tumor after initial surgery. The 3-year-event free survival of the total group was 83+/-2%, and 3-year-overall survival was 92+/-2%. Patients < or=1.5 years had a better outcome than older children. Deletions/imbalances of chromosome 1p were found in 9/90 patients and were associated with a higher event rate but not with a higher death rate. Aberrations of chromosome 11q in 14/91 patients were correlated with a higher event and death rate. Multivariate analysis identified…

AdultRiskOncologyCancer Researchmedicine.medical_specialtyPathologyMultivariate analysisAdolescentBiologyN-Myc Proto-Oncogene ProteinDisease-Free SurvivalNeuroblastomaNeuroblastomaInternal medicinemedicineHumansStage (cooking)ChildRetrospective StudiesChromosome AberrationsOncogene ProteinsN-Myc Proto-Oncogene ProteinChromosomes Human Pair 11Mortality rateInfant NewbornInfantNuclear ProteinsChromosomeRetrospective cohort studySingle copymedicine.diseaseOncologyChromosomes Human Pair 1Child PreschoolCancer Letters
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Small round blue cell sarcoma of bone mimicking atypical Ewing's sarcoma with neuroectodermal features. An analysis of five cases with immunohistoche…

1987

Ewing's sarcoma (ES) of bone may occasionally display rosette-like textures mimicking Homer-Wright ones, as seen in neuroectodermic neoplasms (neuroblastoma, peripheral neuroepithelioma). Of a group of 39 cases of ES, reviewed with electron microscopic study, the authors have isolated five atypical ES, which histologically also possessed neuroectodermic traces. These tumors were composed of small round blue cells with rosette-like figures and cytoplasmic glycogen. The immunohistochemical analysis showed positivity for neuron-specific enolase (NSE) as well as for HNK-1 (leu-7) monoclonal antibody. Electron microscopic examination confirmed the tumor cell as being of small round type, with a …

Antigens Differentiation T-LymphocyteCancer ResearchPathologymedicine.medical_specialtyEnolaseBone NeoplasmsSarcoma EwingBiologylaw.inventionNeuroblastomaPeripheral Nervous System NeoplasmslawNeuroblastomamedicineNeuroectodermal Tumors Primitive PeripheralIntermediate filamentHistocytochemistryAntibodies MonoclonalSoft tissueAnatomymedicine.diseaseMicroscopy ElectronOncologyCytoplasmPhosphopyruvate HydrataseAntigens SurfaceImmunologic TechniquesMicroscopy Electron ScanningImmunohistochemistrySarcomaElectron microscopeGlycogenCancer
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1p36 deletion results in a decrease in glycosaminoglycans which is associated with aggressiveness in neuroblastic tumors

2018

Despite our deep understanding of neuroblastic tumors, some patients still suffer treatment failure, so pre-treatment risk stratification still requires improvement and the search for new therapeutic targets must continue. Here we correlated prognostic clinical and biological features of neuroblastic tumors with the density of extracellular matrix glycosaminoglycans (the main components of the extracellular matrix ‘ground substance’), in nearly 400 primary samples. We also studied the relationship between the density of extracellular matrix glycosaminoglycans and the expression of B3GALT6, an enzyme required for their synthesis. We associated a decrease in glycosaminoglycans with neuroblast…

B3GALT6Neuroblastoma1p36 deletionTherapeutic targetHistologia:6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología [CDU]TumorsGlycosaminoglycans
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H7, a protein kinase C inhibitor, increases the glutathione content of neuroblastoma cells

1992

AbstractIt is shown that the intracellular glutathione (GSH) concentration of neuroblastoma-2a cells in culture increases with a maximum at 24 h after starting treatment with 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H7), an inhibitor of protein kinase C (PKC). Other inhibitors of this and other protein kinases, e.g. sphingosine, staurosporine, and HA 1004, at the concentrations tested, had a less marked or negligible effect on intracellular GSH concentration. 12-O-Tetradecanoylphorbol-13-acetate (TPA) was also tested and showed no significant effect 24 h after addition.

BiophysicsBiologyBiochemistryPiperazinesCellular differentiationchemistry.chemical_compoundMiceNeuroblastomaAlkaloidsStructural BiologySphingosineProtein kinase C1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineGeneticsmedicineTumor Cells CulturedStaurosporineAnimalsNeuroblastoma cellMolecular BiologyProtein kinase CSulfonamidesSphingosineKinaseCell BiologyGlutathioneIsoquinolinesStaurosporineMolecular biologyGlutathioneEnzyme ActivationBiochemistrychemistryEnzyme inhibitor1-(5-Isoquinolinylsulfonyl)-2-methylpiperazine1-(5-Isoquinolinesulfonyl)-2-Methylpiperazinebiology.proteinH7Intracellularmedicine.drugFEBS Letters
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DHEA-Bodipy–a functional fluorescent DHEA analog for live cell imaging

2009

International audience; The androgen dehydroepiandrosterone (DHEA) has been reported to protect neuronal cells against dysfunction and apoptosis. Several signaling pathways involved in these effects have been described but little is known about the intracellular trafficking of DHEA. We describe design, synthesis and characterization of DHEA-Bodipy, a novel fluorescent DHEA analog. DHEA-Bodipy proved to be a functional DHEA derivative: DHEA-Bodipy (i) induced estrogen receptor α-mediated gene activation, (ii) protected PC12 rat pheochromocytoma cells against serum deprivation-induced apoptosis, and (iii) induced stress fibers and focal adhesion contacts in SH-SY5Y human neuroblastoma cells. …

Boron CompoundsDHEA-Bodipyendocrine systemDehydroepiandrosteroneEstrogen receptorApoptosisBiologyPC12 CellsBiochemistryfluorescence microscopyCell membranegenomicNeuroblastoma03 medical and health sciences0302 clinical medicineEndocrinologynon-genomicGenes ReporterLive cell imagingtraffickingmedicinepolycyclic compoundsAnimalsHumansskin and connective tissue diseasesMolecular BiologyFluorescent Dyes030304 developmental biology0303 health sciencesMolecular StructureCell MembraneEstrogen Receptor alphaBiological TransportDehydroepiandrosteroneRats3. Good healthCell biologylive cell imagingmedicine.anatomical_structureMicroscopy FluorescenceApoptosisSignal transductionEstrogen receptor alphahuman activities030217 neurology & neurosurgeryIntracellularhormones hormone substitutes and hormone antagonists
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Cyclic AMP-mediated upregulation of the expression of neuronal NO synthase in human A673 neuroepithelioma cells results in a decrease in the level of…

2004

The expression level of neuronal nitric oxide synthase (nNOS) can vary depending on the (patho)physiological conditions. Here we document a marked induction of nNOS mRNA, protein, and total NO production in response to dibutyryl cyclic AMP (db-cAMP) in human A673 neuroepithelial cells. However, the upregulation of nNOS was associated with a decreased level of production of bioactive NO and by an increase in the level of generation of reactive oxygen species (ROS). ROS production could be prevented by the NOS inhibitor L-NAME, suggesting nNOS itself is involved in ROS generation. Sepiapterin supplementation of db-cAMP-treated A673 cells could restore full bioactive NO production, most likely…

CAMP-Responsive Element ModulatorNitric Oxide Synthase Type IBiologyCREBNitric OxideBiochemistryAdenylyl cyclaseCyclic AMP Response Element Modulatorchemistry.chemical_compoundMiceNeuroblastomaCoactivatorComplement C3b Inactivator ProteinsCyclic AMPAnimalsHumansNeuroectodermal Tumors Primitive PeripheralCREB-binding proteinEnzyme InhibitorsProtein kinase AeducationCyclic AMP Response Element-Binding ProteinGTP CyclohydrolaseCAMP response element bindingHomeodomain ProteinsNeuronseducation.field_of_studyForskolinPhosphoric Diester HydrolasesIntracellular Signaling Peptides and ProteinsBlood ProteinsLIM Domain ProteinsMolecular biologyCyclic AMP-Dependent Protein KinasesPterinsUp-RegulationDNA-Binding ProteinsRepressor ProteinsAntisense Elements (Genetics)NG-Nitroarginine Methyl EsterchemistryBucladesineGene Expression RegulationComplement Factor Hbiology.proteinNitric Oxide SynthaseReactive Oxygen SpeciesSignal TransductionBiochemistry
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MYCN gain and MYCN amplification in a stage 4S neuroblastoma.

2003

Abstract Stage 4S neuroblastoma is a disease associated with spontaneous regression and good survival. We present a patient whose evolution has shown the variety and complexity of this disease in infants. Biologic factors, such as ploidy, MYCN copy number, loss of 1p36, and other chromosomal gains and losses were determined. A complex pattern of genetic abnormalities, such as near-diploidy, MYCN gain (2–4 copies per haploid genome) and imbalance/deletion of 1p36 was seen in the diagnostic sample. An extensive disseminated disease after a latent period of 26 months was associated with a special genetic evolution, such as tetraploidy, MYCN amplification (2:100–500 copies), 1p36 deletion, and …

Cancer ResearchAdrenal Gland NeoplasmsGenes mycDiseaseBiologymedicine.disease_causeNeuroblastomaFatal OutcomeNeuroblastomaGene duplicationGeneticsmedicineHumansneoplasmsMolecular BiologyNeoplasm StagingGeneticsMutationTransition (genetics)Gene AmplificationInfantmedicine.diseaseAneuploidyPrimary tumorChromosomes Human Pair 1Stage 4S NeuroblastomaCancer researchDisease ProgressionFemalePloidyChromosome DeletionChromosomes Human Pair 17Cancer genetics and cytogenetics
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MYCN sensitizes human neuroblastoma to apoptosis by HIPK2 activation through a DNA damage response.

2010

Abstract MYCN amplification occurs in approximately 20% of human neuroblastomas and is associated with early tumor progression and poor outcome, despite intensive multimodal treatment. However, MYCN overexpression also sensitizes neuroblastoma cells to apoptosis. Thus, uncovering the molecular mechanisms linking MYCN to apoptosis might contribute to designing more efficient therapies for MYCN-amplified tumors. Here we show that MYCN-dependent sensitization to apoptosis requires activation of p53 and its phosphorylation at serine 46. The p53S46 kinase HIPK2 accumulates on MYCN expression, and its depletion by RNA interference impairs p53S46 phosphorylation and apoptosis. Remarkably, MYCN ind…

Cancer ResearchApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein-Serine-Threonine KinaseAtaxia Telangiectasia Mutated ProteinNeuroblastomaCell Cycle ProteinSerinePhosphorylationNuclear ProteinOncogene Proteinseducation.field_of_studyN-Myc Proto-Oncogene ProteinAntibiotics AntineoplasticKinaseOncogene ProteinNuclear ProteinsDNA-Binding ProteinsOncologyPhosphorylationRNA InterferenceHumanDNA damageDNA-Binding ProteinPopulationBlotting WesternBiologyProtein Serine-Threonine KinasesN-Myc Proto-Oncogene ProteinBleomycinNeuroblastomaCell Line TumormedicineHumanseducationneoplasmsMolecular BiologyTumor Suppressor ProteinTumor Suppressor ProteinsApoptosimedicine.diseaseTumor progressionApoptosisMutationCancer researchTumor Suppressor Protein p53Carrier ProteinCarrier ProteinsDNA DamageMolecular cancer research : MCR
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Expression of type I interferon receptor and its relation with other prognostic factors in human neuroblastoma.

1998

Expression of type I interferon receptor (IFN-R) has been found in several normal tissues and in malignant neoplasms, mainly those with epithelial differentiation. In order to analyze the immunohistochemical expression of type I IFN-R we studied 79 cases of neuroblastoma. Results of expression of type I IFN-R were statistically correlated with histopathology, stage, bcl-2 and PCNA expression, N-myc amplification and apoptosis. We found expression of type I IFN-R in 54/79 cases showing statistical correlation with bcl-2 expression (P=0.017) and favourable histopathology (P=0.015). The overexpression found in ganglion cells suggests that IFN-R could be involved in the pathway of neuroblastoma…

Cancer ResearchCellular differentiationmedicine.medical_treatmentGenes mycAlpha interferonApoptosisReceptor Interferon alpha-betaBiologyImmunoenzyme TechniquesNeuroblastomaProliferating Cell Nuclear AntigenNeuroblastomaGene expressionBiomarkers TumormedicineHumansChildInterferon alfaNeoplasm StagingReceptors InterferonOncogeneGene AmplificationInfantMembrane ProteinsCell DifferentiationGeneral MedicinePrognosismedicine.diseaseNeoplasm ProteinsCytokineProto-Oncogene Proteins c-bcl-2OncologySpainChild PreschoolCancer researchImmunohistochemistrymedicine.drugOncology Reports
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Abstract 4107: Targeted re-sequencing of neuroblastoma tumors reveals chromosomal rearrangements that involve the Anaplastic Lymphoma Kinase (ALK) ge…

2013

Abstract Neuroblastoma (NBL) is a cancer of early childhood arising from the developing sympathetic nervous system. NBL tumors display a broad clinical and biological heterogeneity, ranging from highly aggressive tumors with fatal outcome to tumors with spontaneous regression. Recurrent mutations are mainly only observed in Anaplastic Lymphoma Kinase (ALK), which is involved in the pathogenesis of both familiar and sporadic NBL. ALK encodes a tyrosine kinase receptor with importance in neuronal development and was initially characterized in anaplastic large cell lymphoma from a translocation leading to the NPM-ALK fusion protein. Subsequent studies show that additional ALK chimeras have bee…

Cancer ResearchChromosomal translocationBiologyAmpliconmedicine.diseaseFusion proteinMolecular biologyExonOncologyhemic and lymphatic diseasesNeuroblastomamedicineAnaplastic lymphoma kinaseKinase activityAnaplastic large-cell lymphomaCancer Research
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