Search results for "N-MYC"

showing 10 items of 36 documents

Targeting MYCN in Pediatric and Adult Cancers

2021

The deregulation of theMYCfamily of oncogenes, includingc-MYC,MYCNandMYCLoccurs in many types of cancers, and is frequently associated with a poor prognosis. The majority of functional studies have focused onc-MYCdue to its broad expression profile in human cancers. The existence of highly conserved functional domains betweenMYCNandc-MYCsuggests thatMYCNparticipates in similar activities.MYCencodes a basic helix-loop-helix-leucine zipper (bHLH-LZ) transcription factor (TF) whose central oncogenic role in many human cancers makes it a highly desirable therapeutic target. Historically, as a TF, MYC has been regarded as “undruggable”. Thus, recent efforts focus on investigating methods to indi…

Cancer ResearchCancercofactorReviewSynthetic lethalityMYCBiologymedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPediatric cancerlcsh:RC254-282pediatric cancerOncologyTranscription (biology)MYCNCancer researchmedicinecancerFunctional studiesSuper-enhancer (SE)Transcription factorPsychological repressionN-Mycneoplasmstranscription factorFrontiers in Oncology
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Exon-level expression analyses identify MYCN and NTRK1 as major determinants of alternative exon usage and robustly predict primary neuroblastoma out…

2012

BACKGROUND: Using mRNA expression-derived signatures as predictors of individual patient outcome has been a goal ever since the introduction of microarrays. Here, we addressed whether analyses of tumour mRNA at the exon level can improve on the predictive power and classification accuracy of gene-based expression profiles using neuroblastoma as a model. METHODS: In a patient cohort comprising 113 primary neuroblastoma specimens expression profiling using exon-level analyses was performed to define predictive signatures using various machine-learning techniques. Alternative transcript use was calculated from relative exon expression. Validation of alternative transcripts was achieved using q…

Cancer ResearchMedizinComputational biologyBiologyexon arraysBioinformaticsN-Myc Proto-Oncogene ProteinExonNeuroblastomaRisk FactorsNeuroblastomaCell Line TumorGene expressionmedicineHumansRNA MessengerReceptor trkAGeneSurvival analysisOncogene ProteinsN-Myc Proto-Oncogene ProteinGene Expression ProfilingInfantNuclear ProteinsGenetics and GenomicspredictionExonsalternative transcript usemedicine.diseasePrognosisSurvival AnalysisGene expression profilingOncologyChild PreschoolPAMDNA microarray
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MYCN and survivin cooperatively contribute to malignant transformation of fibroblasts

2013

The oncogenes MYCN and survivin (BIRC5) maintain aggressiveness of diverse cancers including sarcomas. To investigate whether these oncogenes cooperate in initial malignant transformation, we transduced them into Rat-1 fibroblasts. Indeed, survivin enhanced MYCN-driven contact-uninhibited and anchorage-independent growth in vitro. Importantly, upon subcutaneous transplantation into mice, cells overexpressing both instead of either one of the oncogenes generated tumors with shortened latency, marked anaplasia and an increased proliferation-to-apoptosis ratio resulting in accelerated growth. Mechanistically, the increased tumorigenicity was associated with an enhanced Warburg effect and a hyp…

Cancer ResearchSurvivinBlotting WesternApoptosisBiologyReal-Time Polymerase Chain ReactionN-Myc Proto-Oncogene ProteinInhibitor of Apoptosis ProteinsMalignant transformationImmunoenzyme TechniquesMiceAdenosine TriphosphateSurvivinmedicineAnimalsHumansLactic AcidRNA MessengerneoplasmsAnaplasiaCells CulturedCell ProliferationHomeodomain ProteinsOncogene ProteinsN-Myc Proto-Oncogene ProteinReverse Transcriptase Polymerase Chain ReactionCell growthNuclear ProteinsGeneral MedicineFibroblastsWarburg effectCell HypoxiaRatsTransplantationCell Transformation NeoplasticGlucoseHypoxia-inducible factorsCancer researchmedicine.symptomGlycolysisCarcinogenesis
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Influence of segmental chromosome abnormalities on survival in children over the age of 12 months with unresectable localised peripheral neuroblastic…

2014

Background: The prognostic impact of segmental chromosome alterations (SCAs) in children older than 1 year, diagnosed with localised unresectable neuroblastoma (NB) without MYCN amplification enrolled in the European Unresectable Neuroblastoma (EUNB) protocol is still to be clarified, while, for other group of patients, the presence of SCAs is associated with poor prognosis. Methods: To understand the role of SCAs we performed multilocus/pangenomic analysis of 98 tumour samples from patients enrolled in the EUNB protocol. Results: Age at diagnosis was categorised into two groups using 18 months as the age cutoff. Significant difference in the presence of SCAs was seen in tumours of patients…

Cancer Researchmedicine.medical_specialtyPathologyMYCN AmplificationKaplan-Meier EstimateunresectableGastroenterologyDisease-Free Survivalsegmental chromosome alterationsNeuroblastomaneuroblastomaDDX1FISHaCGHOlder patientsPeripheral Nervous System NeoplasmsInternal medicineNeuroblastomaMYCNmedicineHumansMultiplex ligation-dependent probe amplificationGainChromosome AberrationsOncogene ProteinsComparative Genomic HybridizationN-Myc Proto-Oncogene Proteinbusiness.industrySignificant differenceGene AmplificationSegmental Chromosome abnormalitiesInfantNuclear ProteinsChromosomePrognosislocalisedmedicine.diseaseDoenças GenéticasMLPA3. Good healthPeripheralOncologyMycn amplificationClinical StudyHistopathologybusinessBritish Journal of Cancer
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The Epithelial Mesenchymal Transition Process in Wilms Tumor

2011

Background Until now, only a few mouse-transplanted human tumors or experimental Wilms tumor (WT) cell lines have been described. The aim of this study was to show the biological behavior, including histology, immunohistochemistry (IHC), and molecular biology, of a WT including the original tumor and metastasis transferred into nude mice and followed for successive generations in xenografts. Methods A WT metastasis was xenotransplanted into nude mice and the mice was monitored for 7 passages over a period of 29 months; the original neoplasm was comparatively studied. The morphology was evaluated by optical and electron microscopy. The protein expression was analyzed by immunohistochemistry …

Epithelial-Mesenchymal TransitionHistologyDNA Mutational AnalysisMice NudeCell Growth ProcessesWilms TumorBone and BonesPathology and Forensic MedicineMetastasisMicemedicineAnimalsHumansEpithelial–mesenchymal transitionNeoplasm MetastasisOncogene ProteinsN-Myc Proto-Oncogene ProteinTissue microarrayChemistryMesenchymal stem cellNuclear ProteinsEye Diseases HereditaryWilms' tumorHistologyStriated muscle cell differentiationMicroarray Analysismedicine.diseaseImmunohistochemistryXenograft Model Antitumor AssaysKidney NeoplasmsWnt ProteinsRadiusMedical Laboratory TechnologyMutationCancer researchImmunohistochemistrySignal TransductionApplied Immunohistochemistry & Molecular Morphology
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Galectin-3 Impairment of MYCN-Dependent Apoptosis-Sensitive Phenotype Is Antagonized by Nutlin-3 in Neuroblastoma Cells

2012

MYCN amplification occurs in about 20-25% of human neuroblastomas and characterizes the majority of the high-risk cases, which display less than 50% prolonged survival rate despite intense multimodal treatment. Somehow paradoxically, MYCN also sensitizes neuroblastoma cells to apoptosis, understanding the molecular mechanisms of which might be relevant for the therapy of MYCN amplified neuroblastoma. We recently reported that the apoptosis-sensitive phenotype induced by MYCN is linked to stabilization of p53 and its proapoptotic kinase HIPK2. In MYCN primed neuroblastoma cells, further activation of both HIPK2 and p53 by Nutlin-3 leads to massive apoptosis in vitro and to tumor shrinkage an…

Galectin 3Cancer TreatmentGene Dosagelcsh:MedicineApoptosisProtein-Serine-Threonine KinaseBiochemistryPiperazineschemistry.chemical_compoundNeuroblastoma0302 clinical medicineMolecular Cell BiologyBasic Cancer ResearchSignaling in Cellular Processeslcsh:ScienceEnergy-Producing OrganellesApoptotic SignalingNuclear ProteinOncogene Proteins0303 health sciencesN-Myc Proto-Oncogene ProteinMultidisciplinaryCell DeathImidazolesOncogene ProteinNuclear ProteinsTransfectionNutlin3. Good healthGene Expression Regulation NeoplasticProtein TransportCell killingPhenotypeOncologyGalectin-3030220 oncology & carcinogenesisGene Knockdown TechniquesMedicineResearch ArticleSignal TransductionHumanBiologyBioenergeticsProtein Serine-Threonine KinasesN-Myc Proto-Oncogene ProteinModels Biological03 medical and health sciencesNeuroblastomaCell Line TumormedicineHumansBiologyImidazolePiperazineneoplasms030304 developmental biologylcsh:RGene AmplificationChemotherapy and Drug Treatmentmedicine.diseasechemistryCell cultureApoptosisPediatric OncologyCytoprotectionGene Knockdown TechniqueCancer researchlcsh:QTumor Suppressor Protein p53Carrier ProteinsCarrier ProteinDNA Damage
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How to minimise the effect of tumour cell content in detection of aberrant genetic markers in neuroblastoma

2011

Background: Clinical heterogeneity reflects the complexity of genetic events associated with neuroblastoma (NB). To identify the status of all described genetic loci with possible prognostic interest, high-throughput approaches have been used, but only with tumour cell content >60%. In some tumours, necrotic, haemorrhagic and/or calcification areas influence the low amount of neuroblasts. We evaluated the effect of tumour cell content in the detection of relevant aberrant genetic markers (AGM) diagnosed by fluorescence in situ hybridisation (FISH) on tissue microarrays (TMA) in NB. Methods: Two hundred and thirty-three MYCN non-amplified primary NB included in 12 TMAs were analysed. Results…

Genetic MarkersMaleCancer ResearchPathologymedicine.medical_specialtyShort CommunicationCellBiologyneuroblastomaFISHaberrant genetic markersNeuroblastomatumour cell contentGene duplicationmedicineHumansNuclear proteinneoplasmsIn Situ Hybridization FluorescenceNeoplasm StagingOncogene ProteinsN-Myc Proto-Oncogene Proteinmedicine.diagnostic_testGene AmplificationChromosome MappingInfantNuclear Proteinsprognostic factorsCancerPrognosismedicine.diseaseSurvival Ratemedicine.anatomical_structureOncologyTissue Array AnalysisGenetic markerFemaleNeoplasm stagingFluorescence in situ hybridizationBritish Journal of Cancer
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Analysis of biological prognostic factors using tissue microarrays in neuroblastic tumors

2009

Background Neuroblastic tumors (NT) are pediatric neoplasms with a heterogeneous genetic profile. They present genotypic alterations of prognostic value, the study of which is mandatory in designing therapeutic management. Tissue microarrays (TMA) from paraffin material allow the analysis of a large number of cases with minimal costs. The main purpose of the present study is to analyze specific genetic markers of neuroblastic tumors included in TMAs and determine their prognostic value. We compare the results obtained by different molecular techniques at different substrates to evaluate the feasibility of these assays. Procedure One hundred thirty-nine samples were included in four differen…

Genetic MarkersMalePathologymedicine.medical_specialtyDiseaseN-Myc Proto-Oncogene ProteinNeuroblastomaRisk FactorsGenotypeHumansMedicineStage (cooking)ChildRetrospective StudiesOncogene ProteinsN-Myc Proto-Oncogene ProteinTissue microarraybusiness.industryAge FactorsNuclear ProteinsCell DifferentiationRetrospective cohort studyHematologyPrognosisNeuroblastic TumorTreatment OutcomeOncologyTissue Array AnalysisGenetic markerMutationPediatrics Perinatology and Child HealthFemalebusinessPediatric Blood & Cancer
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Immunohistochemical Study as a Tool in Differential Diagnosis of Pediatric Malignant Rhabdoid Tumor

2010

Malignant rhabdoid tumors (MRTs) are aggressive childhood neoplasms, occurring mainly in the kidney and brain. We describe 2 unusual cases of extrarenal and noncranial location (liver and soft tissue with dissemination) mimicking hepatoblastoma, neuroblastoma or Ewing sarcoma. Both cases revealed a polyphenotypic profile, combined with cytokeratin, vimentin, and CD99 expression. INI1/BAF-47 showed negative protein nuclear expression in both cases, suggesting a diagnosis of MRT. An extensive immunohistochemical panel was performed to exclude pediatric tumors reminiscent of MRT. The genetic studies failed to detected MYCN amplification, 11q23 deletion, and EWS break-apart positivity. No alter…

HepatoblastomaPathologymedicine.medical_specialtySkin NeoplasmsHistologyDesmoplastic small-round-cell tumorChromosomal Proteins Non-HistoneCD9912E7 AntigenN-Myc Proto-Oncogene ProteinPathology and Forensic MedicineDiagnosis DifferentialNeoplasms Multiple PrimaryFatal OutcomeAntigens CDNeuroblastomaAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansVimentinRhabdoid TumorChromosome AberrationsOncogene ProteinsN-Myc Proto-Oncogene Proteinbusiness.industryLiver NeoplasmsInfant NewbornInfantNuclear ProteinsWilms' tumorSMARCB1 Proteinmedicine.diseaseImmunohistochemistryDNA-Binding ProteinsMedical Laboratory TechnologyDrug Resistance NeoplasmKeratinsFemaleSarcomaRNA-Binding Protein EWSDifferential diagnosisbusinessCell Adhesion MoleculesTranscription FactorsApplied Immunohistochemistry & Molecular Morphology
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The genetic tumor background is an important determinant for heterogeneous MYCN ‐amplified neuroblastoma

2016

Amplification of MYCN is the signature genetic aberration of 20–25% of neuroblastoma and a stratifying marker associated with aggressive tumor behavior. The detection of heterogeneous MYCN amplification (hetMNA) poses a diagnostic dilemma due to the uncertainty of its relevance to tumor behavior. Here, we aimed to shed light on the genomic background which permits hetMNA in neuroblastoma and tied the occurrence to other stratifying markers and disease outcome. We performed SNP analysis using Affymetrix Cytoscan HD arrays on 63 samples including constitutional DNA, tumor, bone marrow and relapse samples of 26 patients with confirmed hetMNA by MYCN‐FISH. Tumors of patients ≤18m were mostly an…

Male0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyTumor Markers and Signaturesuniparental disomyAdolescentMYCN amplificationAneuploidyBiologyPolymorphism Single NucleotideN-Myc Proto-Oncogene ProteinBenign tumorGenetic HeterogeneityNeuroblastoma03 medical and health sciences0302 clinical medicineNeuroblastomamedicineHumansChildIn Situ Hybridization FluorescenceChromosome AberrationsOncogene ProteinsN-Myc Proto-Oncogene ProteinGenetic heterogeneityGene AmplificationInfantNuclear ProteinsAneuploidymedicine.diseaseUniparental disomy030104 developmental biologyOncologyChild Preschool030220 oncology & carcinogenesisintratumoral heterogeneityCancer researchFemaleChromosome DeletionTrisomySNP arrayInternational Journal of Cancer
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