[FLT3突变的急性髓性白血病的发病机制和治疗]。

Yuichi Ishikawa
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摘要

FLT3 突变是成人急性髓性白血病(AML)患者中最常发现的基因异常,约占 30%。FLT3-ITD突变被认为是急性髓细胞白血病的不良预后因素,建议年轻患者在首次缓解期进行异基因造血细胞移植。据报道,近期临床引入的FLT3抑制剂可改善FLT3突变阳性急性髓细胞性白血病患者的预后。在日本,除了对复发/难治患者使用吉特替尼或奎沙替尼单药治疗外,奎沙替尼联合强化化疗也于2023年获批用于未经治疗的FLT3-ITD突变阳性急性髓细胞白血病患者。迄今为止的研究已经证明了针对FLT3突变的可测量/最小残留病评估的实用性以及异基因移植后维持治疗的疗效。不过,也观察到出现了与耐药性相关的其他基因突变。因此,FLT3 突变不仅是急性髓细胞性白血病的预后因素,也是治疗和反应评估的目标。此外,涉及 FLT3 抑制剂的新治疗策略的开发有望改善 FLT3 突变阳性急性髓细胞性白血病患者的临床疗效。
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[Pathogenesis and treatment of acute myeloid leukemia with FLT3 mutations].

FLT3 mutations are the most frequently identified genetic abnormalities in adult acute myeloid leukemia (AML) patients, accounting for approximately 30%. FLT3-ITD mutation specifically is considered as a poor prognostic factor in AML, and allogeneic hematopoietic cell transplantation in first remission is recommended for younger patients. The recent clinical introduction of FLT3 inhibitors has been reported to improve the prognosis of patients with FLT3 mutation-positive AML. In Japan, alongside monotherapy with gilteritinib or quizartinib for relapsed/refractory patients, combination of quizartinib with intensive chemotherapy was approved in 2023 for untreated FLT3-ITD mutation-positive AML. Studies to date have demonstrated the utility of measurable/minimal residual disease evaluation targeting FLT3 mutations and the efficacy of maintenance therapy after allogeneic transplantation. However, emergence of additional genetic mutations associated with treatment resistance has been observed. Thus, FLT3 mutations are utilized not only as a prognostic factor in AML but also as a target for treatment and for response assessment. Furthermore, the development of new treatment strategies involving FLT3 inhibitors is highly anticipated to improve clinical outcomes for patients with FLT3 mutation-positive AML.

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