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DNA repair contributes to the drug-resistant phenotype of primary acute myeloid leukaemia cells with FLT3 internal tandem duplications and is reversed by the FLT3 inhibitor PKC412

Hematological MalignancyGenome InstabilityDrug-resistant PhenotypeMixed-phenotype Acute LeukemiaGeneticsMalignant Blood DisorderDna ReplicationFlt3 Inhibitor Pkc412MedicineCell BiologyCancer ResearchDna Repair ContributesMyeloid Neoplasia