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Paper Details

Inhibition of BCL2A1 by STAT5 inactivation overcomes resistance to targeted therapies of FLT3-ITD/D835 mutant AML.
Transl Oncol
10
2022
AML, AML cell lines, BCL2, BCL2A1, BCL2A1 transcription start sites, BET, BRD4, BRD4 binding site, CPI-0610, D835, FLT3, FLT3-ITD, FLT3-ITD/, FLT3-ITD/D835, FLT3-ITD/D835 mutant, FLT3-ITD/D835 mutant AML, FLT3-ITD/D835 mutated AML, FLT3-ITD/D835 positive AML cells, FLT3-mutated AML cells, ITD, ITD/D835, ITD/D835 mutant cells, STAT5, Tyrosine, Tyrosine kinase, acute myeloid leukemia, gilteritinib, primary AML cells, promoter region, quizartinib, tyrosine, tyrosine kinase domain, venetoclax
Author NameAffiliation
Kazuho IkeoCenter for Information Biology, National Institute of Genetics
Wei ZhangThe University of Texas MD Anderson Cancer Center
Wei ZhangThe University of Texas MD Anderson Cancer Center
Bogumil KaczkowskiRIKEN Center for Life Science Technologies
Takashi HatoIndiana University School of Medicine
Yoshihide Hayashizaki
Yoshihide Hayashizaki
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Release 1.2