Acute myeloid leukemia with FMS-like tyrosine kinase-3 (FLT3) mutation

Acute myeloid leukemia with FMS-like tyrosine kinase-3 (FLT3) mutation is an aggressive molecular subtype of acute myeloid leukemia, a hematopoietic malignancy characterized by the rapid proliferation and accumulation of abnormal, immature myeloid blasts in the bone marrow and peripheral blood

Acute myeloid leukemia with FMS-like tyrosine kinase-3 (FLT3) mutation is an aggressive molecular subtype of acute myeloid leukemia, a hematopoietic malignancy characterized by the rapid proliferation and accumulation of abnormal, immature myeloid blasts in the bone marrow and peripheral blood These mutations induce ligand-independent, constitutive activation of downstream signaling cascades, promoting leukemic cell survival, proliferation, and impaired hematopoietic differentiation

Acute myeloid leukemia with FMS-like tyrosine kinase-3 (FLT3) mutation is an aggressive molecular subtype of acute myeloid leukemia, a hematopoietic malignancy characterized by the rapid proliferation and accumulation of abnormal, immature myeloid blasts in the bone marrow and peripheral blood

Primarily affecting adults, this disease is defined by oncogenic activating alterations in the *FLT3* gene—most commonly internal tandem duplications (FLT3-ITD) or point mutations within the tyrosine kinase domain (FLT3-TKD) Clinically, this subtype frequently presents with high circulating blast counts, bone marrow failure resulting in severe cytopenias, and historically elevated risks of relapse and adverse clinical outcomes

Primarily affecting adults, this disease is defined by oncogenic activating alterations in the *FLT3* gene—most commonly internal tandem duplications (FLT3-ITD) or point mutations within the tyrosine kinase domain (FLT3-TKD) Clinically, this subtype frequently presents with high circulating blast counts, bone marrow failure resulting in severe cytopenias, and historically elevated risks of relapse and adverse clinical outcomes

These mutations induce ligand-independent, constitutive activation of downstream signaling cascades, promoting leukemic cell survival, proliferation, and impaired hematopoietic differentiation

These mutations induce ligand-independent, constitutive activation of downstream signaling cascades, promoting leukemic cell survival, proliferation, and impaired hematopoietic differentiation

Clinically, this subtype frequently presents with high circulating blast counts, bone marrow failure resulting in severe cytopenias, and historically elevated risks of relapse and adverse clinical outcomes