Author
Listed:
- Aparna Gorthi
(University of Texas Health at San Antonio
Greehey Children’s Cancer Research Institute, University of Texas Health at San Antonio)
- July Carolina Romero
(University of Texas Health at San Antonio
Greehey Children’s Cancer Research Institute, University of Texas Health at San Antonio)
- Eva Loranc
(Greehey Children’s Cancer Research Institute, University of Texas Health at San Antonio)
- Lin Cao
(Greehey Children’s Cancer Research Institute, University of Texas Health at San Antonio)
- Liesl A. Lawrence
(University of Texas Health at San Antonio
Greehey Children’s Cancer Research Institute, University of Texas Health at San Antonio)
- Elicia Goodale
(Greehey Children’s Cancer Research Institute, University of Texas Health at San Antonio)
- Amanda Balboni Iniguez
(Dana-Farber Cancer Institute and Boston Children’s Hospital, Harvard Medical School
The Broad Institute of MIT and Harvard)
- Xavier Bernard
(University of Texas Health at San Antonio
Greehey Children’s Cancer Research Institute, University of Texas Health at San Antonio)
- V. Pragathi Masamsetti
(Greehey Children’s Cancer Research Institute, University of Texas Health at San Antonio)
- Sydney Roston
(Georgetown University)
- Elizabeth R. Lawlor
(University of Michigan)
- Jeffrey A. Toretsky
(Georgetown University)
- Kimberly Stegmaier
(Dana-Farber Cancer Institute and Boston Children’s Hospital, Harvard Medical School
The Broad Institute of MIT and Harvard)
- Stephen L. Lessnick
(Center for Childhood Cancer and Blood Diseases, Nationwide Children’s Hospital)
- Yidong Chen
(Greehey Children’s Cancer Research Institute, University of Texas Health at San Antonio
Mays Cancer Center, University of Texas Health at San Antonio
University of Texas Health at San Antonio)
- Alexander J. R. Bishop
(University of Texas Health at San Antonio
Greehey Children’s Cancer Research Institute, University of Texas Health at San Antonio
Mays Cancer Center, University of Texas Health at San Antonio)
Abstract
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.
Suggested Citation
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. Lawlo, 2018.
"EWS–FLI1 increases transcription to cause R-loops and block BRCA1 repair in Ewing sarcoma,"
Nature, Nature, vol. 555(7696), pages 387-391, March.
Handle:
RePEc:nat:nature:v:555:y:2018:i:7696:d:10.1038_nature25748
DOI: 10.1038/nature25748
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Cited by:
- Aleix Bayona-Feliu & Emilia Herrera-Moyano & Nibal Badra-Fajardo & Iván Galván-Femenía & María Eugenia Soler-Oliva & Andrés Aguilera, 2023.
"The chromatin network helps prevent cancer-associated mutagenesis at transcription-replication conflicts,"
Nature Communications, Nature, vol. 14(1), pages 1-16, December.
- Heathcliff Dorado García & Fabian Pusch & Yi Bei & Jennifer Stebut & Glorymar Ibáñez & Kristina Guillan & Koshi Imami & Dennis Gürgen & Jana Rolff & Konstantin Helmsauer & Stephanie Meyer-Liesener & N, 2022.
"Therapeutic targeting of ATR in alveolar rhabdomyosarcoma,"
Nature Communications, Nature, vol. 13(1), pages 1-15, December.
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