ETV1 is a lineage survival factor that cooperates with KIT in gastrointestinal stromal tumours
Ping Chi,
Yu Chen,
Lei Zhang,
Xingyi Guo,
John Wongvipat,
Tambudzai Shamu,
Jonathan A. Fletcher,
Scott Dewell,
Robert G. Maki,
Deyou Zheng,
Cristina R. Antonescu,
C. David Allis () and
Charles L. Sawyers ()
Additional contact information
Ping Chi: Memorial Sloan-Kettering Cancer Center
Yu Chen: Memorial Sloan-Kettering Cancer Center
Lei Zhang: Memorial Sloan-Kettering Cancer Center
Xingyi Guo: Albert Einstein College of Medicine, Bronx, New York, 10461 USA
John Wongvipat: Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center
Tambudzai Shamu: Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center
Jonathan A. Fletcher: Brigham and Women’s Hospital
Scott Dewell: Genomics Resource Center, The Rockefeller University
Robert G. Maki: Memorial Sloan-Kettering Cancer Center
Deyou Zheng: Albert Einstein College of Medicine, Bronx, New York, 10461 USA
Cristina R. Antonescu: Memorial Sloan-Kettering Cancer Center
C. David Allis: Laboratory of Chromatin Biology & Epigenetics, The Rockefeller University
Charles L. Sawyers: Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center
Nature, 2010, vol. 467, issue 7317, 849-853
Abstract:
ETV1: a factor in gastrointestinal cancer Gastroinestinal stromal tumours (GISTs) arise in the interstitial cells of Cajal, cells embedded in the musculature of the gastrointestinal tract where they generate electrical rhythmicity. Chi et al. now show that the transcription factor ETV1 is required for the development of these cells, and also promotes tumour development. The KIT gene, often activated by mutations in GIST, cooperates with ETV1 in the transformation of interstitial cells of Cajal, in part by promoting ETV1 stabilization. ETV1 seems to be present in high levels in all GISTs, making it a candidate diagnostic biomarker, and ETV1 blockers may prove useful against drug-resistant GIST.
Date: 2010
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DOI: 10.1038/nature09409
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