Journal
NATURE COMMUNICATIONS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms6794
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Funding
- Fund for Scientific Research-Flanders (FWO-V) [G056813N, 3G002711]
- Belgian Federation for the Study Against Cancer (BFAC)
- European Hematology Association (EHA) [2009/26]
- Australian NHMRC grant [1047995]
- Odysseus type II grant
- FWO-V
- Children Cancer Free Foundation (Stichting Kinderen Kankervrij) [KIKA2008-029]
- Agency for Innovation by Science and Technology (IWT)
- Royal Dutch Academy of Arts and Sciences
- Ligue Contre le Cancer grant programme Carte d'Identite des tumeurs (CIT)
- SLI programme from the French Agence National pour la Recherche
- ERC St-Grant Consolidator [311660-CEVAL]
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Early T-cell precursor leukaemia (ETP-ALL) is a high-risk subtype of human leukaemia that is poorly understood at the molecular level. Here we report translocations targeting the zinc finger E-box-binding transcription factor ZEB2 as a recurrent genetic lesion in immature/ETP-ALL. Using a conditional gain-of-function mouse model, we demonstrate that sustained Zeb2 expression initiates T-cell leukaemia. Moreover, Zeb2-driven mouse leukaemia exhibit some features of the human immature/ETP-ALL gene expression signature, as well as an enhanced leukaemia-initiation potential and activated Janus kinase (JAK)/signal transducers and activators of transcription (STAT) signalling through transcriptional activation of IL7R. This study reveals ZEB2 as an oncogene in the biology of immature/ETP-ALL and paves the way towards pre-clinical studies of novel compounds for the treatment of this aggressive subtype of human T-ALL using our Zeb2-driven mouse model.
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