Can FLT3 inhibitors overcome resistance in AML?

被引:8
|
作者
Tam, Winnie F.
Gilliland, Gary [1 ]
机构
[1] Harvard Univ, Sch Med, Brigham & Womens Hosp, Dept Med, Boston, MA 02115 USA
关键词
FLT3; inhibitors; resistance; staurosporine; midostaurin; PKC412; tandutinib; MLN; 518; lestaurtinib; CEP701; SU11248; AML;
D O I
10.1016/j.beha.2007.11.003
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The identification of FLT3 mutations across a range of the cytogenetic subgroups of AML has opened up the possibility of a targeted therapeutic approach with broad applicability. Four agents are currently in clinical trials, at least 3 of which have both sufficient activity against AML and sufficiently acceptable toxicity profiles to support continued efforts to refine their inclusion into therapeutic regimens for AML. Better understanding of the genetics of inherent and acquired resistance is needed to guide development of second-generation agents. Optimizing the integration of FLT3 inhibitor therapy with chemotherapy has the potential both to decrease toxicity and improve response.
引用
收藏
页码:13 / 20
页数:8
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