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Y. Heshmati et al.
Herein, we demonstrated that CHD4 is essential for maintenance of childhood AML and the LICs that are responsible for the emergence and development of the disease. Our data indicate that the importance of CHD4 in childhood AML may be mediated in part by promoting the expression of the MYC oncogene and its target genes. The cancer-specific dependency found in our studies show that CHD4 may represent a promising therapeutic target to battle childhood AML.
Acknowledgments
We thank Ying Qu for help with RNA-Seq analysis. We also thank Tim Somervaille for kindly providing the MLL-AF9 vec- tor and Marco Herold for kindly providing the Cas9-mCherry vector. We would also like to thank NOPHO and Josefine Palle for providing the primary childhood AML cells as well as
Cecilia Götherström and the National Cord Blood Bank at Karolinska University Hospital for providing the UCBs. We would like to acknowledge the MedH Core Flow Cytometry facility (Karolinska Institutet), supported by KI/SLL, for pro- viding cell sorting services, cell analysis services, technical expertise and scientific input. We would also like to thank the Affymetrix core facility at Neo, BEA, Bioinformatics and Expression Analysis, which is supported by the board of research at the Karolinska Institute and the research committee at the Karolinska hospital.
Funding
This work was supported by the Wallenberg Foundation, The Swedish Cancer Society, the Magnus Bergvalls Foundation, the Karolinska Institutet, the Åke Wibergs Foundation, and Dr Åke Olsson Foundation for Hematological Research.
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