NOTCH1 promotes T cell leukemia-initiating activity by RUNX-mediated regulation of PKC-θ and reactive oxygen species

被引：0
|
作者：
Vincenzo Giambra
Christopher R Jenkins
Hongfang Wang
Sonya H Lam
Olena O Shevchuk
Oksana Nemirovsky
Carol Wai
Sam Gusscott
Mark Y Chiang
Jon C Aster
R Keith Humphries
Connie Eaves
Andrew P Weng
机构：
[1] Terry Fox Laboratory,Department of Pathology
[2] British Columbia Cancer Agency,Division of Hematology/Oncology
[3] Vancouver,undefined
[4] Brigham and Women's Hospital/Harvard Medical School,undefined
[5] Boston,undefined
[6] Massachusetts,undefined
[7] USA.,undefined
[8] University of Michigan Comprehensive Cancer Center,undefined
来源：
Nature Medicine | 2012年 / 18卷
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摘要：
The authors uncover a new mechanism for the regulation of the activity of leukemia-initiating cells in T-ALL. A subpopulation of stem cells with low amounts of reactive oxygen species (ROS) is enriched in their ability to reconstitute disease in mouse models, and this effect is regulated by repression of PKC-θ, which increases ROS production. Moreover, oncogenic NOTCH, a common T-ALL–driving alteration, regulates stem cell activity by increasing RUNX3 expression, which represses RUNX1, a PCK-θ activator, a pathway that is conserved in human patients.
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页码：1693 / 1698
页数：5
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