Oncogenic cooperation between TCF7-SPI1 and NRAS(G12D) requires β-catenin activity to drive T-cell acute lymphoblastic leukemia

SPI1 fusion genes in T-cell acute lymphoblastic leukemia (T-ALL) are commonly found with co-occurring NRAS mutations. Here, the authors show that the combination of these oncogenes is necessary to drive T-ALL in a murine model and that the oncogenic activity of the SPI1 fusion is dependent on β-cate...

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Autores principales: Quentin Van Thillo, Jolien De Bie, Janith A. Seneviratne, Sofie Demeyer, Sofia Omari, Anushree Balachandran, Vicki Zhai, Wai L. Tam, Bram Sweron, Ellen Geerdens, Olga Gielen, Sarah Provost, Heidi Segers, Nancy Boeckx, Glenn M. Marshall, Belamy B. Cheung, Kiyotaka Isobe, Itaru Kato, Junko Takita, Timothy G. Amos, Ira W. Deveson, Hannah McCalmont, Richard B. Lock, Ethan P. Oxley, Maximilian M. Garwood, Ross A. Dickins, Anne Uyttebroeck, Daniel R. Carter, Jan Cools, Charles E. de Bock
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/097bfb27edca4477bb37a09172ff1f71
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Sumario:SPI1 fusion genes in T-cell acute lymphoblastic leukemia (T-ALL) are commonly found with co-occurring NRAS mutations. Here, the authors show that the combination of these oncogenes is necessary to drive T-ALL in a murine model and that the oncogenic activity of the SPI1 fusion is dependent on β-catenin.