0000000000128945

AUTHOR

Heather P. Mcdowell

showing 2 related works from this author

Galectin-3 is a marker of favorable prognosis and a biologically relevant molecule in neuroblastic tumors

2014

Childhood neuroblastic tumors are characterized by heterogeneous clinical courses, ranging from benign ganglioneuroma (GN) to highly lethal neuroblastoma (NB). Although a refined prognostic evaluation and risk stratification of each tumor patient is becoming increasingly essential to personalize treatment options, currently only few biomolecular markers (essentially MYCN amplification, chromosome 11q status and DNA ploidy) are validated for this purpose in neuroblastic tumors. Here we report that Galectin-3 (Gal-3), a β-galactoside-binding lectin involved in multiple biological functions that has already acquired diagnostic relevance in specific clinical settings, is variably expressed in m…

0301 basic medicineMaleCancer ResearchPathologyTime FactorsCellular differentiationGalectin 3ApoptosisPredictive Value of TestKaplan-Meier EstimateNeuroblastoma0302 clinical medicineRisk FactorsChildGanglioneuroblastomaGanglioneuroblastomaCell DifferentiationBlood ProteinsNeuroblastic TumorPhenotypeImmunohistochemistry3. Good healthGalectin-3030220 oncology & carcinogenesisChild PreschoolImmunohistochemistryOriginal ArticleFemaleHumanmedicine.medical_specialtyAdolescentTime FactorSchwannian stromaGalectinsImmunologyBiologyTransfectionNeural cell differentiationschwannian stroma; neuroblastoma prognostic factor; neural cell differentiation; neuroblastoma03 medical and health sciencesCellular and Molecular NeurosciencePredictive Value of TestsNeuroblastomaCell Line TumormedicineBiomarkers TumorCell AdhesionHumansGanglioneuromaNeuroblastoma prognostic factorCell ProliferationNeoplasm StagingRisk FactorInfant NewbornApoptosiInfantGanglioneuromaCell Biologymedicine.disease030104 developmental biologyCancer research
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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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