Nature Communications (Nov 2019)
Myeloid lineage enhancers drive oncogene synergy in CEBPA/CSF3R mutant acute myeloid leukemia
- Theodore P. Braun,
- Mariam Okhovat,
- Cody Coblentz,
- Sarah A. Carratt,
- Amy Foley,
- Zachary Schonrock,
- Brittany M. Smith,
- Kimberly Nevonen,
- Brett Davis,
- Brianna Garcia,
- Dorian LaTocha,
- Benjamin R. Weeder,
- Michal R. Grzadkowski,
- Joey C. Estabrook,
- Hannah G. Manning,
- Kevin Watanabe-Smith,
- Sophia Jeng,
- Jenny L. Smith,
- Amanda R. Leonti,
- Rhonda E. Ries,
- Shannon McWeeney,
- Cristina Di Genua,
- Roy Drissen,
- Claus Nerlov,
- Soheil Meshinchi,
- Lucia Carbone,
- Brian J. Druker,
- Julia E. Maxson
Affiliations
- Theodore P. Braun
- Knight Cancer Institute, Oregon Health & Science University
- Mariam Okhovat
- Knight Cardiovascular Institute, Oregon Health & Science University
- Cody Coblentz
- Knight Cancer Institute, Oregon Health & Science University
- Sarah A. Carratt
- Knight Cancer Institute, Oregon Health & Science University
- Amy Foley
- Knight Cancer Institute, Oregon Health & Science University
- Zachary Schonrock
- Knight Cancer Institute, Oregon Health & Science University
- Brittany M. Smith
- Knight Cancer Institute, Oregon Health & Science University
- Kimberly Nevonen
- Knight Cardiovascular Institute, Oregon Health & Science University
- Brett Davis
- Knight Cardiovascular Institute, Oregon Health & Science University
- Brianna Garcia
- Knight Cancer Institute, Oregon Health & Science University
- Dorian LaTocha
- Knight Cancer Institute, Oregon Health & Science University
- Benjamin R. Weeder
- Program in Molecular and Cellular Biology, Oregon Health & Science University
- Michal R. Grzadkowski
- Computational Biology Program, Oregon Health & Science University
- Joey C. Estabrook
- Computational Biology Program, Oregon Health & Science University
- Hannah G. Manning
- Computational Biology Program, Oregon Health & Science University
- Kevin Watanabe-Smith
- Knight Cancer Institute, Oregon Health & Science University
- Sophia Jeng
- Division of Bioinformatics and Computational Biology, Oregon Health & Science University
- Jenny L. Smith
- Clinical Research Division, Fred Hutchinson Cancer Research Center
- Amanda R. Leonti
- Clinical Research Division, Fred Hutchinson Cancer Research Center
- Rhonda E. Ries
- Clinical Research Division, Fred Hutchinson Cancer Research Center
- Shannon McWeeney
- Knight Cancer Institute, Oregon Health & Science University
- Cristina Di Genua
- MRC Molecular Haematology Unit, MRC Weatherall Institute of Molecular Medicine, John Radcliffe Hospital
- Roy Drissen
- MRC Molecular Haematology Unit, MRC Weatherall Institute of Molecular Medicine, John Radcliffe Hospital
- Claus Nerlov
- MRC Molecular Haematology Unit, MRC Weatherall Institute of Molecular Medicine, John Radcliffe Hospital
- Soheil Meshinchi
- Clinical Research Division, Fred Hutchinson Cancer Research Center
- Lucia Carbone
- Knight Cardiovascular Institute, Oregon Health & Science University
- Brian J. Druker
- Knight Cancer Institute, Oregon Health & Science University
- Julia E. Maxson
- Knight Cancer Institute, Oregon Health & Science University
- DOI
- https://doi.org/10.1038/s41467-019-13364-2
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 15
Abstract
Acute Myeloid Leukemia (AML) develops following multiple mutations of differing impact. Here, the authors show that activating mutations of CSF3R co-operate with loss-of-function mutations of CEBPA to promote AML development through an enhancer-dependent mechanism.