FLT3 mutations in acute myeloid leukemia: a review focusing on clinically applicable drugs

被引:17
作者
Ahn, Jae-Sook [1 ,2 ]
Kim, Hyeoung-Joon [1 ,2 ]
机构
[1] Chonnam Natl Univ, Hwasun Hosp, Dept Internal Med, Gwangju, South Korea
[2] Chonnam Natl Univ, Hwasun Hosp, Genom Res Ctr Hematopoiet Dis, Hwasun, South Korea
关键词
Acute myeloid leukemia; FLT3-ITD; FLT3-TKD; Tyrosine kinase inhibitor; Gilteritinib; Midostaurin; INTERNAL TANDEM DUPLICATION; KINASE DOMAIN MUTATIONS; TYROSINE KINASE; ALLELIC RATIO; NPM1; MUTATION; BONE-MARROW; AML; CHEMOTHERAPY; SORAFENIB; PROGNOSIS;
D O I
10.5045/br.2022.2022017
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
FMS-like tyrosine kinase 3 (FLT3) mutations, the most frequently detected genetic aberrations in patients with acute myeloid leukemia (AML), are identified in approximately 30% of patients with newly diagnosed AML and are more common in patients with normal karyotypes. Since the discovery of FLT3 mutations in AML, clinical trials have been actively conducted in patients with FLT3 mutated AML, and FLT3 inhibitors have been introduced into clinical practice. The current standard treatment for patients with newly diagnosed FLT3-mutated AML is 7+3 induction chemotherapy combined with midostaurin. Additionally, gilteritinib is more effective than salvage chemotherapy for relapsed or refractory FLT3-mutated AML. Ongoing trials are expected to provide additional treatment options depending on the disease state and patient vulnerability. This review summarizes information on clinically available FLT3 inhibitors for the management of AML with FLT3 mutations.
引用
收藏
页码:32 / 36
页数:5
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