ArticleCell stem cell2015
Hematopoietic Differentiation Is Required for Initiation of Acute Myeloid Leukemia.
Article in Cell stem cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
84 citing papers in PubMed, 117 citations in OpenAlex.
- Phf6 truncating mutation drives leukemogenesis via disrupted epigenetic regulation in mice.Leukemia · 2026Article
- Thrombopoietin increases susceptibility for EVI1 + KMT2A-MLLT3-driven AML expressing stem cell genes linked to poor outcome.Nature communications · 2025Article
- Chromatin accessibility in stem cells unveils progressive transcriptional alterations in myelodysplastic syndrome.Nature communications · 2025Article
- Review
- Acute myeloid leukemia with plasmacytoid dendritic cell proliferation: A case report and literature review.Oncology letters · 2025Article
- Learning the cellular origins across cancers using single-cell chromatin landscapes.Nature communications · 2025Article
- Identification and validation of pyroptosis patterns in AML via comprehensive bioinformatics analysis.Discover oncology · 2025Article
- The Crossroads of Clonal Evolution, Differentiation Hierarchy, and Ontogeny in Leukemia Development.Blood cancer discovery · 2025Review
- Article
- Condensate-Promoting ENL Mutation Drives Tumorigenesis In Vivo Through Dynamic Regulation of Histone Modifications and Gene Expression.Cancer discovery · 2024Article
- Article
- C/EBPβ-induced lymphoid-to-myeloid transdifferentiation emulates granulocyte-monocyte progenitor biology.Stem cell reports · 2024Article
- RNA mGenes & diseases · 2024Article
- Exploring the promising potential of induced pluripotent stem cells in cancer research and therapy.Molecular cancer · 2023Review
- PRL2 inhibition elevates PTEN protein and ameliorates progression of acute myeloid leukemia.JCI insight · 2023Article
- Progressive disruption of hematopoietic architecture from clonal hematopoiesis to MDS.iScience · 2023Article
- Carm1-arginine methylation of the transcription factor C/EBPα regulates transdifferentiation velocity.eLife · 2023Article
- Targeting C/EBPα overcomes primary resistance and improves the efficacy of FLT3 inhibitors in acute myeloid leukaemia.Nature communications · 2023Article
- IMPDH inhibition activates TLR-VCAM1 pathway and suppresses the development of MLL-fusion leukemia.EMBO molecular medicine · 2023Article
- Inhibiting the biogenesis of myeloid-derived suppressor cells enhances immunotherapy efficacy against mammary tumor progression.The Journal of clinical investigation · 2022Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 5 countries.
Funding
Abstract
Mutations in acute myeloid leukemia (AML)-associated oncogenes often arise in hematopoietic stem cells (HSCs) and promote acquisition of leukemia stem cell (LSC) phenotypes. However, as LSCs often share features of lineage-restricted progenitors, the relative contribution of differentiation status to LSC transformation is unclear. Using murine MLL-AF9 and MOZ-TIF2 AML models, we show that myeloid differentiation to granulocyte macrophage progenitors (GMPs) is critical for LSC generation. Disrupting GMP formation by deleting the lineage-restricted transcription factor C/EBPa blocked normal granulocyte formation and prevented initiation of AML. However, restoring myeloid differentiation in C/EBPa mutants with inflammatory cytokines reestablished AML transformation capacity. Genomic analyses of GMPs, including gene expression and H3K79me2 profiling in conjunction with ATAC-seq, revealed a permissive genomic environment for activation of a minimal transcription program shared by GMPs and LSCs. Together, these findings show that myeloid differentiation is a prerequisite for LSC formation and AML development, providing insights for therapeutic development.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.