The role of constitutive activation of FMS-related tyrosine kinase-3 and NRas/KRas mutational status in infants with KMT2A-rearranged acute lymphoblastic leukemia

Constitutive activation of the FMS-related tyrosine kinase-3 (FLT3) by mutations or high expression levels is common in acute leukemias.[1][1] Aberrant FLT3 signaling is mediated via the RAS/MAPK and PI-3-Kinase/AKT pathways leading to proliferation, survival, and therapy resistance.[1][1] Infants