Mechanisms of resistance to targeted therapies for relapsed or refractory acute myeloid leukemia

被引:8
|
作者
Kropp, Erin M. [1 ]
Li, Qing [1 ,2 ]
机构
[1] Univ Michigan Ann Arbor, Dept Internal Med, Ann Arbor, MI USA
[2] Univ Michigan Ann Arbor, 109 Zina Pitcher Pl,BSRB1520, Ann Arbor, MI 48109 USA
基金
美国国家卫生研究院;
关键词
TYROSINE KINASE INHIBITOR; BH3 MIMETIC ABT-737; FLT3; INHIBITORS; PROMOTES LEUKEMOGENESIS; HEMATOPOIETIC STEM; CLINICAL ACTIVITY; MUTATIONS; AML; CHEMOTHERAPY; CELLS;
D O I
10.1016/j.exphem.2022.04.001
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Acute myeloid leukemia (AML) is an aggressive disease of clonal hematopoiesis with a high rate of relapse and refractory disease despite intensive therapy. Traditionally, relapsed or refractory AML has increased therapeutic resistance and poor long-term survival. In recent years, advancements in the mechanistic understanding of leukemogenesis have allowed for the development of targeted therapies. These therapies offer novel alternatives to intensive chemotherapy and have prolonged survival in relapsed or refractory AML. Unfortunately, a significant portion of patients do not respond to these therapies and relapse occurs in most patients who initially responded. This review focuses on the mechanisms of resistance to targeted therapies in relapsed or refractory AML.(c) 2022 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:13 / 24
页数:12
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