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Acknowledgements
We thank Dr. Kevin Shannon for advice and discussions. We thank the Saint-Louis Hospital’s Tumor Biobank (Daniela Geromin, Carole Albuquerque) for managing patient AML samples. This research was supported with grants from the US National Cancer Institute (NCI) (NIH R35 CA210030; KS), the Children’s Leukemia Research Foundation (CLRF), and the Bridge Project, a collaboration between the Koch Institute for Integrative Cancer Research at MIT and the Dana-Farber–Harvard Cancer Center (DF–HCC) (KS and MTH). KS is a Leukemia and Lymphoma Society Scholar. AP is a recipient of support from the ERC Starting Grant (H2020), the ATIP–AVENIR and LNCC French research programs, the EHA research grant for a Non-Clinical Advanced fellow, and is supported by the St. Louis Association for leukemia research. LB is an MD-PhD candidate of “Ecole de l’INSERM Liliane Bettencourt” and a recipient of Philippe Foundation and GPM fellowships.
Author contributions
LB developed the study, established conditions for in vivo and in vitro experiments, acquired and analyzed the data, and wrote the manuscript. GA performed statistical analysis, biostatistics, and computational analysis of the RNAseq data and mined publicly available databases. AS performed in vitro experiments. ER, JS, and RI provided patient samples. OH and MTH designed experiments and helped interpreting data. AP and KS supervised the study, wrote and revised the manuscript, designed the in vitro and in vivo experiments and analyzed the data, provided material and funding support for the study.
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Benajiba, L., Alexe, G., Su, A. et al. Creatine kinase pathway inhibition alters GSK3 and WNT signaling in EVI1-positive AML. Leukemia 33, 800–804 (2019). https://doi.org/10.1038/s41375-018-0291-x
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DOI: https://doi.org/10.1038/s41375-018-0291-x
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