Upregulation of Bcl-2 Confers Resistance to FLT3 Inhibition in FLT3ITD AML with Secondary Acquired Mutations

被引：3

作者：

Yamatani, Kotoko ^{[1
]}

Tabe, Yoko ^{[2
,3
,4
]}

Saito, Kaori ^{[1
]}

Yang, Haeun ^{[1
,5
]}

Murakami-Tonami, Yuko ^{[1
]}

Suzuki, Koya ^{[1
,6
]}

Zhang, Weiguo ^{[7
]}

Kinjo, Sonoko ^{[8
]}

Ikeo, Kazuho ^{[8
]}

Mogushi, Kaoru ^{[9
,10
]}

Hosoya, Masaki ^{[10
,11
]}

Yamaguchi, Shigeo ^{[11
]}

Harada, Hironori ^{[12
]}

Miida, Takashi ^{[1
]}

Shah, Neil P. ^{[13
]}

Konopleva, Marina Y. ^{[14
]}

Hayashizaki, Yoshihide ^{[15
]}

Andreeff, Michael ^{[14
]}

机构：

[1] Juntendo Univ, Grad Sch Med, Dept Clin Lab Med, Tokyo, Japan

[2] Juntendo Univ, Dept Clin Lab Med, Sch Med, Tokyo, Japan

[3] Juntendo Univ, Grad Sch Medcine, Dept Next Generat Hematol Lab Med, Tokyo, Japan

[4] Univ Texas MD Anderson Canc Ctr, Sect Mol Hematol & Therapy, Dept Leukemia, Houston, TX 77030 USA

[5] Juntendo Univ, Grad Sch Med, Leading Ctr Dev & Res Canc Med, Tokyo, Japan

[6] Juntendo Univ, Res Inst Dis Old Age, Grad Sch Med, Tokyo, Japan

[7] Univ Texas MD Anderson Canc Ctr, Houston, TX 77030 USA

[8] Natl Inst Genet, Ctr Informat Biol, Shizuoka, Japan

[9] Juntendo Univ, Grad Sch Med, Dept Diagnost & Therapeut Intractable Dis, Tokyo, Japan

[10] Juntendo Univ, Grad Sch Med, Intractable Dis Res Ctr, Tokyo, Japan

[11] Juntendo Univ, Sch Med, Dept Oncol, Tokyo, Japan

[12] Juntendo Univ, Grad Sch Med, Dept Hematol, Tokyo, Japan

[13] Univ Calif San Francisco, Div Hematol Oncol, San Francisco, CA 94143 USA

[14] Univ Texas MD Anderson Canc Ctr, Dept Leukemia, Sect Leukemia Biol Res, Houston, TX 77030 USA

[15] RIKEN, Ctr Life Sci Technoligies, Prevent Med & Diag Innovat Program, Yokohama, Kanagawa, Japan

来源：

BLOOD | 2018年 / 132卷

关键词：

D O I：

10.1182/blood-2018-99-109957

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

3944

引用

页数：2

共 50 条

[1] FLT3 INHIBITION OVERCOMES RESISTANCE TO THE BCL-2 SELECTIVE ANTAGONIST, VENETOCLAX, IN FLT3-ITD MUTANT AML MODELS
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[2] Pediatric AML primary samples with FLT3/ITD mutations are preferentially killed by FLT3 inhibition
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[8] FLT3-ITD activation mediates resistance to the BCL-2 selective antagonist, venetoclax, in FLT3-ITD mutant AML models
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[10] Glutaminolysis is a metabolic dependency in FLT3ITD acute myeloid leukemia unmasked by FLT3 tyrosine kinase inhibition
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