ArticleNature communications2019
Myeloid lineage enhancers drive oncogene synergy in CEBPA/CSF3R mutant acute myeloid leukemia.
Erratum issuedOpen access · goldAbstract read
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Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 27 papers.
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0cells of the map it votes in
27citing papers in PubMed
2.6field-weighted citation impact, top 9% of its field
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- Trial
- Article
- In Silico Perturbation Identifies Transcription Factors as Protective Targets in HSPCs After Irradiation.International journal of molecular sciences · 2026Article
- Colony-Stimulating Factor 3 Receptor Mutations and Variants in Hematological Malignancies.Cancers · 2025Review
- Research progress on the mechanisms of CSF3R mutations in leukemogenesis and treatment strategies.Cancer cell international · 2025Review
- A review of C/EBP α: a potential novel target for solid tumor intervention.Journal of translational medicine · 2025Review
- Screening for Antileukemia Agents in FMS-like Tyrosine Kinase 3 (FLT3)-Mutated Acute Myeloid Leukemia Cells.ACS pharmacology & translational science · 2025Article
- Metabolomic and transcriptomic remodeling of bone marrow myeloid cells in response to maternal obesity.American journal of physiology. Endocrinology and metabolism · 2025Article
- Multiomics Integration and Machine Learning Reveal Colony Stimulating Factor 3 Receptor as a Key Gene and Therapeutic Target in Crohn's Disease.Mediators of inflammation · 2025Article
- Distribution of different classes of CSF3R mutations and co-mutational pattern in 360 myeloid neoplasia.Annals of hematology · 2025Article
- CEBPA mutations in acute myeloid leukemia: implications in risk stratification and treatment.International journal of hematology · 2024Review
- Article
- Homodimer-mediated phosphorylation of C/EBPα-p42 S16 modulates acute myeloid leukaemia differentiation through liquid-liquid phase separation.Nature communications · 2023Article
- TET2 lesions enhance the aggressiveness of CEBPA-mutant acute myeloid leukemia by rebalancing GATA2 expression.Nature communications · 2023Article
- Clonal evolution and hierarchy in myeloid malignancies.Trends in cancer · 2023Review
- RUNX1::ETO translocations must precede CSF3R mutations to promote acute myeloid leukemia development.Leukemia · 2023Article
- Integrative profiling of gene expression and chromatin accessibility elucidates specific transcriptional networks in porcine neutrophils.Frontiers in genetics · 2023Article
- Article
- Review
- A systematic analysis of genetic interactions and their underlying biology in childhood cancer.Communications biology · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
28 authors at 5 institutions in 2 countries.
Theodore P BraunKnight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA.ORCID http://orcid.org/0000-0002-6248-2143
Mariam OkhovatKnight Cardiovascular Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Cody CoblentzKnight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Sarah A CarrattKnight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA.ORCID http://orcid.org/0000-0003-2493-6789
Amy FoleyKnight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Zachary SchonrockKnight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Brittany M CurtissKnight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Kimberly NevonenKnight Cardiovascular Institute, Oregon Health & Science University, Portland, OR, 97239, USA.ORCID http://orcid.org/0000-0003-0198-1624
Brett DavisKnight Cardiovascular Institute, Oregon Health & Science University, Portland, OR, 97239, USA.ORCID http://orcid.org/0000-0001-7985-1921
Brianna GarciaKnight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Dorian LaTochaKnight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Benjamin R WeederProgram in Molecular and Cellular Biology, Oregon Health & Science University, Portland, OR, 97239, USA.ORCID http://orcid.org/0000-0002-4128-5861
Michal R GrzadkowskiComputational Biology Program, Oregon Health & Science University, Portland, OR, 97239, USA.
Joey C EstabrookComputational Biology Program, Oregon Health & Science University, Portland, OR, 97239, USA.
Hannah G ManningComputational Biology Program, Oregon Health & Science University, Portland, OR, 97239, USA.
Kevin Watanabe-SmithKnight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Sophia JengDivision of Bioinformatics and Computational Biology, Oregon Health & Science University, Portland, OR, 97239, USA.
Jenny L SmithClinical Research Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, Seattle, WA, 98109, USA.
Amanda R LeontiClinical Research Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, Seattle, WA, 98109, USA.
Rhonda E RiesClinical Research Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, Seattle, WA, 98109, USA.
Shannon McWeeneyKnight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA.ORCID http://orcid.org/0000-0001-8333-6607
Cristina Di GenuaMRC Molecular Haematology Unit, MRC Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headley Way, Oxford, OX3 9DS, UK.
Roy DrissenMRC Molecular Haematology Unit, MRC Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headley Way, Oxford, OX3 9DS, UK.ORCID http://orcid.org/0000-0002-8574-5014
Claus NerlovMRC Molecular Haematology Unit, MRC Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headley Way, Oxford, OX3 9DS, UK.ORCID http://orcid.org/0000-0002-0544-735X
Soheil MeshinchiClinical Research Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, Seattle, WA, 98109, USA.
Lucia CarboneKnight Cardiovascular Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Brian J DrukerKnight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA.ORCID http://orcid.org/0000-0001-8331-8206
Julia E MaxsonKnight Cancer Institute, Oregon Health & Science University, Portland, OR, 97239, USA. maxsonj@ohsu.edu.
Oregon Health & Science University · USFred Hutch Cancer Center · USJohn Radcliffe Hospital · GBHoward Hughes Medical Institute · USUniversity of Washington · US
Funding
COG FOREIGN ACCRUALU10CA098543 · NCI · NATIONAL CHILDHOOD CANCER FOUNDATION · PI ADAMSON, PETER C. · 2003 to 2013
$335.5MUpgrade of confocal microscopy at the Oregon National Primate Research CenterP51OD011092 · OD · OREGON HEALTH & SCIENCE UNIVERSITY · PI Bonnie J. Nagel · 2012 to 2026
$203.9MTumor Intrinsic and Microenvironmental Mechanisms Driving Drug Combination Efficacy and Resistance in AMLU54CA224019 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI Jeffrey Wallace Tyner · 2017 to 2026
$13.9MOregon Clinical and Translational Research Institute KL2 SupplementKL2TR002370 · NCATS · OREGON HEALTH & SCIENCE UNIVERSITY · PI Catherine Lee Hough · 2017 to 2026
$10.1MFunctional Genomic Discovery of Pathway Targeted and Immune Modulatory Therapeutic Combinations in Hematologic MalignanciesU01CA217862 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI DRUKER, BRIAN J, TYNER, JEFFREY WALLACE · 2017 to 2021
$5.3MComparative and functional analysis of conservation and rearrangement of topologically associating domains across mammals.R01HG010333 · NHGRI · OREGON HEALTH & SCIENCE UNIVERSITY · PI CARBONE, LUCIA · 2018 to 2021
$2.8MPathogenic Mechanisms of CSF3R Mutations in LeukemiaR00CA190605 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI MAXSON, JULIA E · 2016 to 2018
$733kMedical Research Council G0701761Medical Research Council G0900892Medical Research Council MC_UU_00016/7Medical Research Council MC_UU_12009/7NCATS NIH HHS KL2 TR002370NCI NIH HHS R00 CA190605NCI NIH HHS U01 CA217862NCI NIH HHS U10 CA098543NCI NIH HHS U54 CA224019NHGRI NIH HHS R01 HG010333NIH HHS P51 OD011092
Abstract
Acute Myeloid Leukemia (AML) develops due to the acquisition of mutations from multiple functional classes. Here, we demonstrate that activating mutations in the granulocyte colony stimulating factor receptor (CSF3R), cooperate with loss of function mutations in the transcription factor CEBPA to promote acute leukemia development. The interaction between these distinct classes of mutations occurs at the level of myeloid lineage enhancers where mutant CEBPA prevents activation of a subset of differentiation associated enhancers. To confirm this enhancer-dependent mechanism, we demonstrate that CEBPA mutations must occur as the initial event in AML initiation. This improved mechanistic understanding will facilitate therapeutic development targeting the intersection of oncogene cooperativity.
Indexed as
AnimalsCCAAT-Enhancer-Binding ProteinsCell DifferentiationCell LineageHumansK562 CellsLeukemia, Myeloid, AcuteLoss of Function MutationMiceMutationReceptors, Colony-Stimulating FactorCCAAT-Enhancer-Binding ProteinsCEBPA protein, humanCEBPA protein, mouseCSF3R protein, humanCsf3r protein, mouseReceptors, Colony-Stimulating Factor
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Read underepoch 390
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.