Access through your institution Buy or subscribe However, although AML1–ETO is believed to significantly contribute to leukemogenesis, it was shown that this chimeric protein by itself is

not sufficient to cause leukemia.5 Thus, the search for ‘second hits’ in t(8;21) leukemia has become the focus of intense investigations including SNP genomic arrays analysis.6 It could be

demonstrated that the AML1–ETO fusion gene and FLT3 length mutations collaborate in inducing acute leukemia in mice and there is first evidence that the combination of AML1–ETO and JAK2

V617F mutations results in AML.7, 8 Recently, several studies have shown that in core-binding factor AML up to 40% of t(8;21) patients have additional mutations of the _KIT_ gene, while the

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supported by a grant from the Deutsche Krebshilfe (108397 to BH). We thank Dong-Er Zhang, University of California, San Diego, USA for her very helpful comments with this study. AUTHOR

INFORMATION AUTHORS AND AFFILIATIONS * Department of Hematology/Oncology, University of Freiburg Medical Center, Freiburg, Germany B Hackanson, M Abdelkarim & M Lübbert * Laboratory of

Hematology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands J H Jansen Authors * B Hackanson View author publications You can also search for this author inPubMed 

Google Scholar * M Abdelkarim View author publications You can also search for this author inPubMed Google Scholar * J H Jansen View author publications You can also search for this author

inPubMed Google Scholar * M Lübbert View author publications You can also search for this author inPubMed Google Scholar CORRESPONDING AUTHOR Correspondence to M Lübbert. ETHICS DECLARATIONS

COMPETING INTERESTS The authors declare no conflict of interest. RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Hackanson, B., Abdelkarim, M., Jansen,

J. _et al._ NHR4 domain mutations of ETO are probably very infrequent in AML1–ETO positive myeloid leukemia cells. _Leukemia_ 24, 860–861 (2010). https://doi.org/10.1038/leu.2009.291

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