Maintenance therapy for FLT3-ITD-mutated acute myeloid leukemia

被引：51

作者：

Burchert, Andreas ^{[1
,2
]}

机构：

[1] Philipps Univ Marburg, Dept Internal Med Hematol Oncol & Immunol, Marburg, Germany

[2] Univ Hosp Giessen & Marburg, Campus Marburg, Marburg, Germany

来源：

HAEMATOLOGICA | 2021年 / 106卷 / 03期

关键词：

INTERNAL TANDEM DUPLICATION; KINASE INHIBITOR; CELL TRANSPLANTATION; MIDOSTAURIN PKC412; FLT3; INHIBITORS; STEM-CELLS; SORAFENIB; MUTATIONS; CHEMOTHERAPY; TARGET;

D O I：

10.3324/haematol.2019.240747

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

FLT3-ITD is a constitutively activated variant of the FLT3 tyrosine kinase receptor. Its expression in acute myeloid leukemia (AML) is associated with a poor prognosis. Due to this, the development of tyrosine kinase inhibitors (TKI) blocking FLT3-ITD became a rational therapeutic concept. This review describes key milestones in the clinical development of different FLT3-specific TKI with a particular focus on FLT3-TKI maintenance therapy in remission after allogeneic hematopoietic stem cell transplantation (HCT). Recent evidence from randomized trials using sorafenib in FLT3-ITD mutat ed AML provided a proof of concept that targeted post-HCT maintenance therapy could become a new treatment paradigm in AML.

引用

页码：664 / 670

页数：7

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