FLT3基因在急性髓细胞白血病中的研究现状

Research status on FLT3 gene in acute myeloid leukemia

FMS样酪氨酸激酶(FLT)3基因编码的蛋白是一种Ⅲ型酪氨酸激酶受体,在造血细胞的生长、增殖和分化过程中发挥重要作用。FLT3基因突变是原发性急性髓细胞白血病(AML)中最常见的基因突变,初诊AML患者的FLT3突变发生率约为30%。伴FLT3基因突变的AML患者对常规化疗和异基因造血干细胞移植治疗常疗效不佳,预后较差。FLT3抑制剂可在一定程度上提升该类患者的疗效和预后,但是并非所有患者均能临床获益。FLT3基因突变特征及FLT3抑制剂的作用机制、疗效和耐药方面的研究成果对于改善AML患者的预后和生存质量,具有重要的临床意义。笔者拟就FLT3基因突变在AML中的研究现状进行阐述,以期更好的指导伴FLT3突变AML患者的临床诊疗。

FMS like tyrosine kinase(FLT)3 gene encoded protein is a typeⅢtyrosine kinase receptor that plays an important role in hematopoietic cell survival,proliferation and differentiation.Mutation of the FLT3 gene is the most frequent genetic alteration in patients with primary acute myeloid leukemia(AML),accounting for approximately 30%of newly diagnosed AML patients.AML patients with FLT3 gene mutations are often poorly treated with conventional chemotherapy and allogeneic hematopoietic stem cell transplantation and have a poor prognosis.The emergence of FLT3 kinase inhibitors has greatly improved the survival and prognosis of such patients to a certain extent,but they do not have good therapeutic efficacy for all patients.Studies on the characterization of FLT3 gene mutations,as well as the mechanism,efficacy and drug resistance of FLT3 inhibitors have important clinical significance for improving the prognosis and quality of survival of AML patients.This article elaborates on the current research status of FLT3 gene mutation in AML,in order to better guide the clinical diagnosis and treatment of AML patients with FLT3 gene mutations.