The Future of Targeting FLT3 Activation in AML

被引：36

作者：

Leick, Mark B. ^{[1
]}

Levis, Mark J. ^{[2
]}

机构：

[1] Johns Hopkins Univ, Dept Med, 600 North Wolfe St,Harvey 805, Baltimore, MD 21287 USA

[2] Sidney Kimmel Comprehens Canc Ctr Johns Hopkins, Dept Oncol, 1650 Orleans St,Canc Res Bldg 1,Room 2M44, Baltimore, MD 21287 USA

来源：

CURRENT HEMATOLOGIC MALIGNANCY REPORTS | 2017年 / 12卷 / 03期

关键词：

Acute myeloid leukemia (AML); FLT3; Tyrosine-kinase inhibitor (TKI); ACUTE MYELOID-LEUKEMIA; INTERNAL TANDEM DUPLICATION; STEM-CELL TRANSPLANTATION; ACUTE PROMYELOCYTIC LEUKEMIA; TYROSINE KINASE INHIBITOR; PHASE I/II TRIAL; PROGNOSTIC-SIGNIFICANCE; MYELODYSPLASTIC SYNDROME; MYELOGENOUS LEUKEMIA; LESTAURTINIB CEP701;

D O I：

10.1007/s11899-017-0381-2

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Internal tandem duplications (ITD) and tyrosine-kinase domain (TKD) mutations of the FMS-like tyrosine-kinase 3 (FLT3) can be found in up to one third of patients with acute myeloid leukemia (AML) and confer a poor prognosis. First discovered 20 years ago, these mutations were identified as viable therapeutic targets, and FLT3 tyrosine-kinase inhibitors (TKIs) have been in development for the last decade with steadily increasing potency. However, FLT3-mutated AML often acquires resistance to the growing armamentarium of FLT3 inhibitors through a variety of mechanisms. In this review, we discuss the distinct clinical phenotype of FLT3-mutated AML, historically and currently available therapeutics, mechanisms of resistance, ongoing trials, and future outlook at treatment strategies.

引用

页码：153 / 167

页数：15

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