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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Nature Publishing Group
2021-07-01
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| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/s41467-021-24442-9 |
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doaj-097bfb27edca4477bb37a09172ff1f712021-07-11T11:43:34ZengNature Publishing GroupNature Communications2041-17232021-07-0112111510.1038/s41467-021-24442-9Oncogenic cooperation between TCF7-SPI1 and NRAS(G12D) requires β-catenin activity to drive T-cell acute lymphoblastic leukemiaQuentin Van Thillo0Jolien De Bie1Janith A. Seneviratne2Sofie Demeyer3Sofia Omari4Anushree Balachandran5Vicki Zhai6Wai L. Tam7Bram Sweron8Ellen Geerdens9Olga Gielen10Sarah Provost11Heidi Segers12Nancy Boeckx13Glenn M. Marshall14Belamy B. Cheung15Kiyotaka Isobe16Itaru Kato17Junko Takita18Timothy G. Amos19Ira W. Deveson20Hannah McCalmont21Richard B. Lock22Ethan P. Oxley23Maximilian M. Garwood24Ross A. Dickins25Anne Uyttebroeck26Daniel R. Carter27Jan Cools28Charles E. de Bock29Department of Human Genetics, KU LeuvenDepartment of Human Genetics, KU LeuvenChildren’s Cancer Institute, UNSW Sydney, Lowy Cancer Research CentreDepartment of Human Genetics, KU LeuvenChildren’s Cancer Institute, UNSW Sydney, Lowy Cancer Research CentreChildren’s Cancer Institute, UNSW Sydney, Lowy Cancer Research CentreChildren’s Cancer Institute, UNSW Sydney, Lowy Cancer Research CentreTechnology Innovation Lab, VIBDepartment of Human Genetics, KU LeuvenDepartment of Human Genetics, KU LeuvenDepartment of Human Genetics, KU LeuvenDepartment of Human Genetics, KU LeuvenLeuvens Kanker Instituut (LKI), KU Leuven – UZ LeuvenDepartment of Oncology, KU LeuvenChildren’s Cancer Institute, UNSW Sydney, Lowy Cancer Research CentreChildren’s Cancer Institute, UNSW Sydney, Lowy Cancer Research CentreDepartment of Pediatrics, Graduate School of Medicine, Kyoto UniversityDepartment of Pediatrics, Graduate School of Medicine, Kyoto UniversityDepartment of Pediatrics, Graduate School of Medicine, Kyoto UniversityKinghorn Centre for Clinical Genomics, Garvan Institute of Medical ResearchKinghorn Centre for Clinical Genomics, Garvan Institute of Medical ResearchChildren’s Cancer Institute, UNSW Sydney, Lowy Cancer Research CentreChildren’s Cancer Institute, UNSW Sydney, Lowy Cancer Research CentreAustralian Centre for Blood Diseases, Monash UniversityAustralian Centre for Blood Diseases, Monash UniversityAustralian Centre for Blood Diseases, Monash UniversityLeuvens Kanker Instituut (LKI), KU Leuven – UZ LeuvenChildren’s Cancer Institute, UNSW Sydney, Lowy Cancer Research CentreDepartment of Human Genetics, KU LeuvenChildren’s Cancer Institute, UNSW Sydney, Lowy Cancer Research CentreSPI1 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.https://doi.org/10.1038/s41467-021-24442-9 |
| collection |
DOAJ |
| language |
English |
| format |
Article |
| sources |
DOAJ |
| author |
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 |
| spellingShingle |
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 Oncogenic cooperation between TCF7-SPI1 and NRAS(G12D) requires β-catenin activity to drive T-cell acute lymphoblastic leukemia Nature Communications |
| author_facet |
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 |
| author_sort |
Quentin Van Thillo |
| title |
Oncogenic cooperation between TCF7-SPI1 and NRAS(G12D) requires β-catenin activity to drive T-cell acute lymphoblastic leukemia |
| title_short |
Oncogenic cooperation between TCF7-SPI1 and NRAS(G12D) requires β-catenin activity to drive T-cell acute lymphoblastic leukemia |
| title_full |
Oncogenic cooperation between TCF7-SPI1 and NRAS(G12D) requires β-catenin activity to drive T-cell acute lymphoblastic leukemia |
| title_fullStr |
Oncogenic cooperation between TCF7-SPI1 and NRAS(G12D) requires β-catenin activity to drive T-cell acute lymphoblastic leukemia |
| title_full_unstemmed |
Oncogenic cooperation between TCF7-SPI1 and NRAS(G12D) requires β-catenin activity to drive T-cell acute lymphoblastic leukemia |
| title_sort |
oncogenic cooperation between tcf7-spi1 and nras(g12d) requires β-catenin activity to drive t-cell acute lymphoblastic leukemia |
| publisher |
Nature Publishing Group |
| series |
Nature Communications |
| issn |
2041-1723 |
| publishDate |
2021-07-01 |
| description |
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. |
| url |
https://doi.org/10.1038/s41467-021-24442-9 |
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