grant
Role of p21 positive senescent cells in radiation-induced skeletal injury and repair
Organization MAYO CLINIC ROCHESTERLocation ROCHESTER, UNITED STATESPosted 1 Aug 2023Deadline 30 Apr 2028
NIHUS FederalResearch GrantFY2025AP20187AbscissionAcuteAdipocytesAdipose CellAdverse ExperienceAdverse eventAffectAgingApoptosisApoptosis PathwayArchitectureBiological MarkersBiology of AgingBlood PlasmaBone FormationBone MarrowBone Marrow Blood-Deriving CellBone Marrow Blood-Forming CellBone Marrow CellsBone Marrow Reticuloendothelial SystemCD11bCDK Inhibitor ProteinCDK4ICDKI ProteinCDKN2CDKN2 GenesCDKN2ACDKN2A geneCMM2CR3ACancer SurvivorCaspaseCaspase GeneCell AgingCell BodyCell SenescenceCell Senescence InductionCell-Death ProteaseCellsCellular AgingCellular SenescenceChemotactic CytokinesChronicClinical ResearchClinical StudyCre-LoxCre-LoxPCre/LoxPCrossbreedingCyclin Kinase InhibitorCyclin-Dependent Kinase InhibitorCyclin-Dependent Kinase Inhibitor 2A GeneCysteine EndopeptidasesCysteine ProteaseCysteine ProteinasesCytometryDNA DamageDNA InjuryDasatinibDataDeteriorationDysfunctionEarly InterventionElderlyEngineering / ArchitectureEnvironmentEnzyme GeneEnzymesExcisionExpression SignatureExtirpationFat CellsFibrosisFractureFracture HealingFunctional disorderGene ExpressionGene Expression ProfileGeneralized GrowthGenerationsGeneticGenetic HybridizationGrowthGrowth AgentsGrowth FactorGrowth SubstancesHematopoieticHomologous Chemotactic CytokinesICE-like proteaseINK4INK4AITGAMITGAM geneIn Situ HybridizationIndependent LivingInflammatoryIntercrinesKnowledgeLOXLOX geneLipocytesMAC1AMO1AMTS1MTS1 GenesMature LipocyteMature fat cellMediatingMesenchymalMiceMice MammalsMouse StrainsMurineMusMyeloid CellsNatureNon-Polyadenylated RNAOsteoblastsOsteocytesOsteogenesisOsteoporosisOxidative StressPathway interactionsPatientsPatternPhysiologicPhysiologicalPhysiopathologyPlasmaPlasma SerumPopulationProgrammed Cell DeathProteinsProteins Growth FactorsQOLQuality of lifeQuercetinRNARNA Gene ProductsRadiationRadiation therapyRadiotherapeuticsRadiotherapyRemovalReplicative SenescenceReticuloendothelial System, Serum, PlasmaRibonucleic AcidRisk ReductionRoleSIS cytokinesSeminalStromal CellsSurgical RemovalTP16TSG9ATestingTimeTissue GrowthTransgenesTransgenic MiceVisualizationWorkadvanced ageagedaged miceaged mousebio-markersbiologic markerbiomarkerbiomarker identificationbonebone cellbone fracturebone fracture healingbone fracture repairbone tissue formationcell typecellular aging inductioncellular senescence inductionchemoattractant cytokinechemokinecystein proteasecystein proteinasecysteine endopeptidasecytokineelderly micefracture repairfracture riskfunctional restorationgene expression patterngene expression signaturegeriatrichealinghemopoieticidentification of biomarkersidentification of new biomarkersin situ Hybridization Geneticsin situ Hybridization Staining Methodinjury and repairlong-term recoverymarker identificationnovelold miceontogenyp14ARFp16 Genesp16INK4 Genesp16INK4A Genesp16INK4apathophysiologypathwaypharmacologicpreventpreventingradiation treatmentreduce riskreduce risksreduce that riskreduce the riskreduce these risksreduces riskreduces the riskreducing riskreducing the riskregenerativereplicative agingresectionresponserestore functionrestore functionalityrestore lost functionrisk-reducingsenescencesenescence and its associated secretory phenotypesenescence associated secretomesenescence associated secretory factorssenescence associated secretory pathwaysenescence associated secretory phenotypesenescence associated secretory programsenescence associated secretory proteinssenescence inductionsenescentsenescent associated secretomesenescent associated secretory phenotypesenescent cellsenior citizensenolyticsskeletalskeletal injurysocial rolestemstressortheoriestherapeutic targettranscriptional profiletranscriptional signaturetransgenetreatment with radiation
Description preview
Project Summary/Abstract
Skeletal deterioration and related fracture risk is exacerbated in the elderly cancer survivors receiving
radiation treatment (RTx), affecting independent living, and reducing quality of life. Cellular senescence, one of
the major pathways induced following RTx-induced DNA damage, is characterized by a pro-inflammatory…
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