EWS–FLI1 increases transcription to cause R-loops and block BRCA1 repair in Ewing sarcoma

被引：0
|
作者：
Aparna Gorthi
July Carolina Romero
Eva Loranc
Lin Cao
Liesl A. Lawrence
Elicia Goodale
Amanda Balboni Iniguez
Xavier Bernard
V. Pragathi Masamsetti
Sydney Roston
Elizabeth R. Lawlor
Jeffrey A. Toretsky
Kimberly Stegmaier
Stephen L. Lessnick
Yidong Chen
Alexander J. R. Bishop
机构：
[1] University of Texas Health at San Antonio,Department of Cell Systems and Anatomy
[2] Greehey Children’s Cancer Research Institute,Department of Pediatric Oncology
[3] University of Texas Health at San Antonio,Departments of Oncology and Pediatrics
[4] Dana-Farber Cancer Institute and Boston Children’s Hospital,Departments of Pediatrics and Pathology
[5] Harvard Medical School,Department of Epidemiology and Biostatistics
[6] The Broad Institute of MIT and Harvard,undefined
[7] Georgetown University,undefined
[8] University of Michigan,undefined
[9] Center for Childhood Cancer and Blood Diseases,undefined
[10] Nationwide Children’s Hospital,undefined
[11] Mays Cancer Center,undefined
[12] University of Texas Health at San Antonio,undefined
[13] University of Texas Health at San Antonio,undefined
来源：
Nature | 2018年 / 555卷
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摘要：
The EWS–FLI1 fusion protein, expressed in Ewing sarcoma, increases global transcription, causes accumulation of R loops and replication stress, and impairs BRCA1-mediated repair.
引用
收藏
页码：387 / 391
页数：4
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