Research Progress of FLT3 Mutation in Acute Myeloid Leukemia --Review.
10.19746/j.cnki.issn.1009-2137.2023.03.046
- Author:
Lu GUO
1
;
Hui-Xia XIONG
2
Author Information
1. Graduate School of Qinghai University,Xining 810000，Qinghai Province，China.
2. Department of Hematology, Nanjing Lishui People's Hospital/Zhong Da Hospital Lishui Branch, Southeast University, Nanjing 211200, Jiangsu Province, China. E-mail: xhx-73@163.com.
- Publication Type:Journal Article
- Keywords:
acute myeloid leukemia;
mechanism of drug resistance
- MeSH:
Humans;
Mutation;
Protein Kinase Inhibitors/therapeutic use*;
Signal Transduction;
Receptor Protein-Tyrosine Kinases/therapeutic use*;
Leukemia, Myeloid, Acute/drug therapy*;
fms-Like Tyrosine Kinase 3/genetics*
- From:
Journal of Experimental Hematology
2023;31(3):922-926
- CountryChina
- Language:Chinese
-
Abstract:
Acute myeloid leukemia (AML) is a heterogeneous hematopoietic tumor originated from hematopoietic stem cells. FLT3 is an important receptor tyrosine kinase in cell signal transduction pathway and one of the common mutated genes in AML. AML patients with FLT3-ITD mutation have a poor prognosis and tendency to relapse. Therefore, early identification of FLT3 gene mutation and selection of appropriate treatment are particularly important. Currently, the small moleculetargeted drugs have been new treatment methods for AML patients with FLT3-ITD mutation, but accompanied drug resistance need to be solved. This paper reviews the mechanism of FLT3 mutation, the clinical significance of FLT3 mutation in AML, FLT3 inhibitors and drug resistance mechanism.
