bioRxiv preprint doi: https://doi.org/10.1101/2020.10.23.352070; this version posted October 23, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Transcriptional silencing of ALDH2 in acute myeloid leukemia confers a dependency on Fanconi anemia proteins Zhaolin Yang1, Yiliang Wei1, Xiaoli S. Wu1,2, Shruti V. Iyer1,2, Moonjung Jung3, Emmalee R. Adelman4, Olaf Klingbeil1, Melissa Kramer1, Osama E. Demerdash1, Kenneth Chang1, Sara Goodwin1, Emily Hodges5, W. Richard McCombie1, Maria E. Figueroa4, Agata Smogorzewska3, and Christopher R. Vakoc1,6* 1Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA 2Genetics Program, Stony Brook University, Stony Brook, New York 11794, USA 3Laboratory of Genome Maintenance, The Rockefeller University, New York 10065, USA 4Sylvester Comprehensive Cancer Center, Miller School of Medicine, University of Miami, Miami, FL 33136, USA 5Department of Biochemistry and Vanderbilt Genetics Institute, Vanderbilt University School of Medicine, Nashville, TN 37232, USA 6Lead contact *Correspondence:
[email protected] Running title: Fanconi anemia pathway dependency in AML Category: Myeloid Neoplasia 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.10.23.352070; this version posted October 23, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Key Points Dependency on the Fanconi anemia (FA) DNA interstrand crosslink repair pathway is identified in AML.