Nature Communications (Jul 2021)

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

  • 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

DOI
https://doi.org/10.1038/s41467-021-24442-9
Journal volume & issue
Vol. 12, no. 1
pp. 1 – 15

Abstract

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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.