FLT3是致癌基因，编码蛋白是一种跨膜受体酪氨酸激酶，其主要在调节造血功能中起作用。FLT3在与其配体FLT3L结合后二聚化和自磷酸化后被激活。FLT3的激活通过几种途径导致下游信号传导，包括MAPK，PI3K / AKT和STAT3 / 5途径，其在造血增殖，分化和存活中具有关键作用。野生型FLT3对于造血干细胞的生长和分化是重要的，并且通常在未成熟骨髓和淋巴样细胞上表达。FLT3改变发生在急性髓性白血病（AML）中，最常见的是在约25％的AML中呈现FLT3内部串联重复（FLT3-ITD）或在约7％的AML中呈现酪氨酸激酶结构域中的点突变。小鼠模型中的FLT3-ITD表达不足以引起白血病发生，然而，额外的致癌改变与FLT3的过度活化合作引起恶性肿瘤。

FLT3 is a transmembrane receptor tyrosine kinase that predominantly functions in the regulation of hematopoiesis. FLT3 is activated following dimerization and autophosphorylation upon binding to its ligand, FLT3L. Activation of FLT3 results in downstream signaling via several pathways including the MAPK, PI3K/AKT and STAT3/5 pathways, which have key roles in hematopoietic proliferation, differentiation and survival. Wildtype FLT3 is important for the growth and differentiation of hematopoietic stem cells and is commonly expressed on immature myeloid and lymphoid cells. FLT3 alterations occur in acute myeloid leukemia (AML), most commonly presenting as FLT3 internal tandem duplications (FLT3-ITD) in about 25% of AMLs or point mutations in the tyrosine kinase domain in about 7% of AMLs. FLT3-ITD expression in murine models is not sufficient to cause leukemogenesis, however, additional oncogenic alterations cooperate with overactivation of FLT3 to cause malignancy.

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