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Targeting vulnerabilities of PPM1D-mutant gliomas
Organization DANA-FARBER CANCER INSTLocation BOSTON, UNITED STATESPosted 1 Feb 2021Deadline 31 Jan 2026 ⚠️
NIHUS FederalResearch GrantFY20250-11 years oldAPF-1ATP-Dependent Proteolysis Factor 1AffectAntioncogene Protein p53ApoptosisApoptosis PathwayAssayAttenuatedBioassayBiologic ModelsBiological AssayBiological ModelsCDS1CHEK1CHEK1 geneCHEK2CHEK2 geneCHK1CHK2CRISPR approachCRISPR based approachCRISPR methodCRISPR methodologyCRISPR techniqueCRISPR technologyCRISPR toolsCRISPR-CAS-9CRISPR-based methodCRISPR-based techniqueCRISPR-based technologyCRISPR-based toolCRISPR/CAS approachCRISPR/Cas methodCRISPR/Cas technologyCRISPR/Cas9CRISPR/Cas9 technologyCSAID-Binding Protein 1CSAID-Binding Protein 2CSBP2Cancer GenesCancer-Promoting GeneCancersCas nuclease technologyCds1 kinaseCell BodyCell Communication and SignalingCell Cycle ArrestCell Cycle CheckpointCell SignalingCell-Cycle Checkpoint KinaseCellsCellular Tumor Antigen P53Checkpoint kinase 1ChildChild YouthChildhood Brain NeoplasmChildhood Brain TumorChildhood GliomaChildren (0-21)Chk2 protein kinaseClustered Regularly Interspaced Short Palindromic Repeats approachClustered Regularly Interspaced Short Palindromic Repeats methodClustered Regularly Interspaced Short Palindromic Repeats methodologyClustered Regularly Interspaced Short Palindromic Repeats techniqueClustered Regularly Interspaced Short Palindromic Repeats technologyCouplingCytokine-Suppressive Antiinflammatory Drug-Binding Protein 1Cytokine-Suppressive Antiinflammatory Drug-Binding protein 2DNADNA DamageDNA InjuryDNA Repair GeneDNA damage check pointDNA damage check point responseDNA damage checkpointDNA damage checkpoint responseDNA mutationDNA repair proteinDataDeoxyribonucleic AcidDependenceDevelopmentDiagnosisEndometrial CancerEndometrial CarcinomaEndometrium CancerEndometrium CarcinomaEsteroproteasesEventFK506 Binding Protein 12-Rapamycin Associated Protein 1FKBP12 Rapamycin Complex Associated Protein 1FRAP1FRAP1 geneFRAP2GenesGeneticGenetic ChangeGenetic defectGenetic mutationGlial Cell TumorsGlial NeoplasmGlial TumorGliomaGliomagenesisGrowth AgentsGrowth FactorGrowth SubstancesHDM2HMG-20High Mobility Protein 20HistonesHumanImmune PrecipitationImmunoprecipitationIn VitroInduced DNA AlterationInduced MutationInduced Sequence AlterationIntracellular Communication and SignalingMAP kinaseMAPK14MAPK14 Mitogen-Activated Protein KinaseMAPK14 geneMDM2MDM2 geneMDMX proteinMalignant NeoplasmsMalignant TumorMass Photometry/Spectrum AnalysisMass SpectrometryMass SpectroscopyMass SpectrumMass Spectrum AnalysesMass Spectrum AnalysisMdm-2 proteinMechanistic Target of RapamycinMetabolic Protein DegradationMitogen-Activated Protein Kinase 14Mitogen-Activated Protein KinasesModel SystemModelingModern ManMutationMxi2Neural Stem CellNeuroglial NeoplasmNeuroglial TumorOncogenesOncogenicOncoprotein MDM2Oncoprotein p53P53PI3K-AlphaPIK3-AlphaPIK3CAPIK3CA genePP1425PPM1DPPM1D genePathway interactionsPatientsPediatric GliomaPediatric high-grade gliomaPeptidasesPeptide HydrolasesPhosphatidylinositol 3-Kinase, Catalytic, 110-kD, AlphaPhosphatidylinositol 3-Kinase, Catalytic, AlphaPhosphoprotein P53Phosphoprotein PhosphatasePhosphoprotein Phosphatase-2CPhosphoprotein PhosphohydrolasePhosphoprotein pp53ProcessProgrammed Cell DeathProliferatingProtease GeneProteasesProtein Phosphatase CProtein Phosphatase GeneProtein Phosphatase-1Protein Phosphatase-2AProtein TP53Protein TurnoverProtein phosphataseProteinasesProteinsProteins Growth FactorsProteolytic EnzymesRAD53RAFT1RadiationRecurrenceRecurrentRegulatory ProteinRegulatory Protein DegradationReporterRoleSAPK2ASecondary toSignal PathwaySignal TransductionSignal Transduction SystemsSignalingStressStress-Activated Protein Kinase 2ATP53TP53 geneTRP53TestingTherapeuticTransforming GenesTumor Protein p53Tumor Protein p53 GeneUbiquitinattenuateattenuatesattenuationbiological signal transductioncell cycle check pointcell-cycle check point kinasecheck point kinase 1check point kinase 2checkpoint kinase 2chk1 kinasechk1 protein kinaseclinical relevanceclinically relevantcombinatorialcurative interventioncurative therapeuticcurative therapycurative treatmentsdevelopmentaldiffuse midline gliomadriver lesiondriver mutationentire genomeexperimentexperimental researchexperimental studyexperimentsfull genomegenetic regulatory proteingenome mutationgenome scalegenome-widegenomewideglial-derived tumorglioma genesisin vivoin vivo ModelinhibitorinsightkidsleukemiamTORmalignancymammalian target of rapamycinmdm-2 oncogene proteinmdm2 proteinmutantneoplasm/cancernerve stem cellneural precursorneural precursor cellneural progenitorneural progenitor cellsneural stem and progenitor cellsneurogenic progenitorsneurogenic stem cellneuroglia neoplasmneuroglia tumorneuron progenitorsneuronal progenitorneuronal progenitor cellsneuronal stem cellsneuroprogenitoroptimismp110-Alphap38p38 MAP Kinasep38 MAPK Genep38 Mitogen Activated Protein Kinasep38 Protein Kinasep38 SAPKp38-Alphap38Alphap53 Antigenp53 Genesp53 Tumor Suppressorp53-Binding Protein MDM2pathwaypatient populationpediatric brain neoplasmpediatric brain tumorphospho-proteomicsphosphoproteomicspositive attitudeprecision medicineprecision-based medicineprogenitor and neural stem cellsprogenitor cell modelprogenitor modelprotein degradationprotein p53regulatory gene productreplication stressresponseserine-threonine-protein kinase Chk2social rolestem and progenitor cell modelstem cell based modelstem cell derived modelstem cell modelstructural mutationstructural variantstructural variationtherapeutic targettumorwhole genomeyoungster
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Project Summary/Abstract
Diffuse midline gliomas (DMGs) are devastating brain tumors of childhood with no curative treatments. We and
others have observed up to 15% of all DMGs to harbor activating mutations in PPM1D which encodes the WIP1
protein phosphatase. Similar mutations are also observed in other cancers, including leukemias and…
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