grant
Genetic and molecular basis for SRSF2 mutations in myelodysplasia
Organization FRED HUTCHINSON CANCER CENTERLocation SEATTLE, UNITED STATESPosted 1 Aug 2015Deadline 30 Apr 2029
NIHUS FederalResearch GrantFY2025AML - Acute Myeloid LeukemiaAcute Myeloblastic LeukemiaAcute Myelocytic LeukemiaAcute Myelogenous LeukemiaAffectAmino AcidsAntigensAvidityAwardBiologicalBloodBlood CellsBlood Reticuloendothelial SystemBody TissuesBone MarrowBone Marrow Reticuloendothelial SystemCD8 CellCD8 T cellsCD8 lymphocyteCD8+ T cellCD8+ T-LymphocyteCD8-Positive LymphocytesCD8-Positive T-LymphocytesCell BodyCell surfaceCellsCharacteristicsCis-Acting LocusCis-Acting SequenceClass I GenesDNA AlterationDNA Sequence AlterationDNA mutationDataDevelopmentDiseaseDisease ProgressionDisorderDissectionDysmyelopoietic SyndromesENX-1EZH1EZH2EZH2 geneElementsEnhancer of Zeste 2 Polycomb Repressive Complex 2 SubunitEnvironmentEventExonsExposure toFundingFutureGene ExpressionGenerationsGenesGeneticGenetic AlterationGenetic ChangeGenetic EngineeringGenetic Engineering BiotechnologyGenetic Engineering Molecular BiologyGenetic defectGenetic mutationHematopoiesisHematopoietic Cellular Control MechanismsHeterozygoteHumanImmuneImmunesImmunotherapeutic agentIn VitroInduced DNA AlterationInduced MutationInduced Sequence AlterationIneffective HematopoiesisInterdisciplinary ResearchInterdisciplinary StudyIntervening SequencesIntronsIsoformsKMT6KMT6AKnowledgeLytotoxicityMHC Class IMHC Class I GenesMHC ReceptorMajor Histocompatibility Complex ReceptorMapsMessenger RNAMethodsMissense MutationModern ManMolecularMultidisciplinary CollaborationMultidisciplinary ResearchMutationMyelodysplastic DiseaseMyelodysplastic SyndromesNon-Polyadenylated RNANormal TissueNormal tissue morphologyPathogenesisPatientsPatternPeptidesPeripheral Blood CellPhenotypePoint MutationPre-Clinical ModelPreclinical ModelsProductionProtein IsoformsProteinsRNARNA BindingRNA Gene ProductsRNA SequencesRNA SplicingRNA boundReagentRecombinant DNA TechnologyRecurrenceRecurrentRefractory Anemia with an Excess of BlastsRefractory anaemia with excess blastsResearch ResourcesResourcesRibonucleic AcidRiskSC35SRSF2SRSF2 geneSamplingSequence AlterationSeriesSerine/Arginine-Rich Splicing Factor 2Smoldering LeukemiaSplicingSurfaceT cell responseT-Cell Antigen ReceptorsT-Cell ReceptorT-CellsT-LymphocyteT-cell receptor repertoireT8 CellsT8 LymphocytesTCR repertoireTechnologyTestingTherapeuticTissuesTrans-Acting FactorsTrans-ActivatorsTransactivatorsTranscriptTreatment EfficacyWorkacute granulocytic leukemiaacute myeloid leukemiaaminoacidantigen-specific T cellsbiologicblood cell formationcell typeclinical developmentcurative interventioncurative therapeuticcurative therapycurative treatmentscytotoxicitydevelopmentalengineered T cellsgain of functiongenetically engineeredgenetically engineered T-cellsgenome mutationgenomic alterationheterozygosityhuman modelimmune drugsimmune-based therapeuticsimmunogenimmunogenicimmunologic therapeuticsimmunotherapeuticsimmunotherapy agentimprovedinsightintervention efficacyloss of functionmRNAmissense single nucleotide polymorphismmissense single nucleotide variantmissense variantmodel of humanmouse modelmurine modelmutantmyelodysplasianative protein drugneo-antigenneo-epitopesneoantigensneoepitopesnew approachesnew drug treatmentsnew drugsnew pharmacological therapeuticnew technologynew therapeutic approachnew therapeutic interventionnew therapeutic strategiesnew therapeuticsnew therapynew therapy approachesnew treatment approachnew treatment strategynext generation therapeuticsnovelnovel approachesnovel drug treatmentsnovel drugsnovel pharmaco-therapeuticnovel pharmacological therapeuticnovel strategiesnovel strategynovel technologiesnovel therapeutic approachnovel therapeutic interventionnovel therapeutic strategiesnovel therapeuticsnovel therapynovel therapy approachpeptide aminoacid sequencepeptide sequencepharmaceutical proteinpreferenceprotein aminoacid sequenceprotein drug agentprotein expressionprotein-based drugsmall moleculesynthetic lethal interactionsynthetic lethalitytherapeutic efficacytherapeutic evaluationtherapeutic proteintherapeutic testingtherapy efficacythymus derived lymphocytetransgenic T- cells
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Description preview
Mutations in genes encoding RNA splicing factors are the single most common class of genetic alterations in
patients with myelodysplastic syndromes (MDS). Recurrent mutations affecting SF3B1, SRSF2, and U2AF1
are the most common and occur as heterozygous point mutations at specific amino acid residues. In the first
two periods of funding of this…
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