grant
Dual Kinase and LSD1 Inhibition in Acute Myeloid Leukemia
Organization OREGON HEALTH & SCIENCE UNIVERSITYLocation PORTLAND, UNITED STATESPosted 13 Jul 2023Deadline 30 Jun 2028
NIHUS FederalResearch GrantFY2025AML - Acute Myeloid LeukemiaAOF2Acute Myeloblastic LeukemiaAcute Myelocytic LeukemiaAcute Myelogenous LeukemiaAutomobile DrivingAvian Myelocytomatosis Viral Oncogene HomologBasal Transcription FactorBasal transcription factor genesBindingCD114CD114 AntigenCSF3RCSF3R geneCell Communication and SignalingCell CycleCell DeathCell Division CycleCell LineCell SignalingCellLineCharacteristicsChromatinClinicalClinical TreatmentClinical TrialsColony Stimulating Factor 3 ReceptorComplexCorrelative StudyDNA mutationDataDevelopmentDiseaseDisorderDrug CombinationsDrug SynergismDrug TargetingDrugsEnhancersEpigeneticEpigenetic ChangeEpigenetic MechanismEpigenetic ProcessEvaluationFLK2FLT3FLT3 geneFLT3 inhibitorFMS-like tyrosine kinase 3Fms-Related Tyrosine Kinase 3G-CSF ReceptorsGCSF ReceptorGCSFRGene ExpressionGeneral Transcription Factor GeneGeneral Transcription FactorsGenesGenetic ChangeGenetic defectGenetic mutationGranulocyte Colony-Stimulating Factor ReceptorsIntracellular Communication and SignalingInvestigationJAK-2JAK2JAK2 geneJAK2 proteinJanus kinase 2KDM1AKDM1A geneKinasesLSD1LinkLysine-Specific Demethylase 1Lysine-Specific Demethylase 1AMEKsMGF proteinMGSNF proteinMYC Family ProteinMYC ProteinMYC geneMalignant CellMediatingMedicationMinorityMolecularMolecular InteractionMutationOncogenicOutcomePDX modelPTK InhibitorsPatient derived xenograftPatientsPharmaceutical PreparationsPhase 1b TrialPhase Ib TrialPhosphotransferase GenePhosphotransferasesPlayProtein Tyrosine Kinase InhibitorsRefractoryRegulationRelapseRepressionResistanceRoleSTAT5STAT5ASTAT5A geneSTAT5a Transcription FactorSTK-1 kinaseSTK1SamplingSignal PathwaySignal Transducer and Activator of Transcription 5ASignal TransductionSignal Transduction SystemsSignalingStat5 proteinStat5a proteinStat5alpha proteinStem Cell Tyrosine Kinase 1Strains Cell LinesTK InhibitorsTestingTherapeuticTranscription Factor Proto-OncogeneTranscription factor genesTranslatingTransphosphorylasesTyrosine Kinase InhibitorTyrosine-Protein Kinase JAK2Workacute granulocytic leukemiaacute granulocytic leukemia cellacute myeloblastic leukemia cellacute myelocytic leukemia cellacute myelogenous leukemia cellacute myeloid leukemiaacute myeloid leukemia cellacute nonlymphocytic leukemia cellantileukemic activitybiological signal transductioncancer cellclinical interventionclinical therapyclinical translationclinically translatablecultured cell linedetermine efficacydevelopmentaldrivingdrug/agenteffective therapyeffective treatmentefficacy analysisefficacy assessmentefficacy determinationefficacy evaluationefficacy examinationepigenetic profilingepigeneticallyevaluate efficacyexamine efficacyexpression subtypesfetal liver kinase-2fetal liver kinase-3genome mutationimprovedinhibitorinhibitor druginhibitor therapeuticinhibitor therapykinase inhibitormammary gland factormammary gland-specific nuclear factormembermolecular sub-typesmolecular subsetsmolecular subtypesmouse modelmurine modelmutantmyc Oncogenesnecrocytosisnew therapeutic approachnew therapeutic interventionnew therapeutic strategiesnew therapy approachesnew treatment approachnew treatment strategynovel therapeutic approachnovel therapeutic interventionnovel therapeutic strategiesnovel therapy approachparticipant enrollmentpatient derived xenograft modelpatient enrollmentpre-clinicalpre-clinical efficacypreclinicalpreclinical efficacyprogramspromoterpromotorresistantresponseresponse to therapyresponse to treatmentsignal tranducer and activator of transcription 5social rolesynergismtherapeutic responsetherapy responsetranscription factortreatment responsetreatment responsivenesstrial regimentrial treatment
Description preview
PROJECT SUMMARY/ABSTRACT
Kinase inhibitor therapy has made a minimal impact on the clinical treatment of patients with Acute Myeloid
Leukemia (AML). We have shown that inhibition of the epigenetic regulator lysine-specific demethylase 1 (LSD1)
augments the efficacy of kinase inhibition in AML, including drugs targeting FLT3, cKIT and JAK2. This…
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