AC220 and AraC cause differential inhibitory dynamics in patient-derived M5-AML with FLT3-ITD and, thus, ultimately distinct therapeutic outcomes

Author:

An Xiaoyu,Liu Jinping,Wang Na,Wang Di,Huang Liang,Zhang Likun,Cai Jie,Wery Jean-Pierre,Zhou Demin,Zhou Jianfeng,Li Qi-Xiang

Publisher

Elsevier BV

Subject

Cancer Research,Cell Biology,Genetics,Hematology,Molecular Biology

Reference25 articles.

1. Role of FLT3 in leukemia;Gilliland;Curr Opin Hematol,2002

2. Internal tandem duplication of the flt3 gene found in acute myeloid leukemia;Nakao;Leukemia,1996

3. Mutant FLT3: A direct target of sorafenib in acute myelogenous leukemia;Zhang;J Natl Cancer Inst,2008

4. Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia;Smith;Nature,2012

5. AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML);Zarrinkar;Blood,2009

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