Investigating oncogenic FMS-like tyrosine kinase 3 (FLT3)-induced metabolic reprogramming in acute myeloid leukaemia

Abstract

Mutations in the FMS-like tyrosine kinase 3 (FLT3) gene are among the most frequently occurring somatic mutations in acute myeloid leukaemia (AML), a disease that presents with devastating prognosis. FLT3 is primarily expressed on hematopoietic progenitor cells, and during early haematopoiesis coordinates a ligand-dependent signalling cascade that regulates the proliferation and maturation of the progenitor pool. FLT3 internal tandem duplication (FLT3-ITD), the most common type of FLT3 mutation, promotes constitutive FLT3 kinase activity and hyperactivation of downstream signalling pathways including STAT5, PI3K/mTOR and MAPK. Though our understanding of the molecular pathways downstream of ..