ArticleNature genetics2019
Subtype-specific regulatory network rewiring in acute myeloid leukemia.
Article in Nature genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.
What it found
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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.
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Who cites it
131 citing papers in PubMed, 195 citations in OpenAlex.
- Genetic deletion of JAM-C in preleukemic cells rewires leukemic stem cell gene expression program in AML.Blood advances · 2024Trial
- Single-cell chromatin profiling reveals relapse-related priming in pediatric acute myeloid leukemia.Life science alliance · 2026Article
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- Article
- Disrupting a Convergent Acetylation Circuit Collapses Leukemic Identity Across AML Subtypes.bioRxiv : the preprint server for biology · 2026Article
- Inhibition of p300/CREBBP catalytic activity drives context-dependent transcriptional activation in AML.Blood · 2026Article
- Understanding drug resistance in chronic myeloid leukemia through the lens of leukemic stem cell states: insights from single-cell analyses.Haematologica · 2026Review
- Article
- Sustained MYC overexpression drives myeloid differentiation block and acquisition of leukemic phenotypes.Experimental hematology · 2026Article
- Multiomic Profiling Reveals the Regulation of Many Immune-Related Genes by PU.1 in Porcine Alveolar Macrophages.Animals : an open access journal from MDPI · 2026Article
- Transcriptomic validation of a 7,12 Dimethylbenz(a)anthracene (DMBA)-induced leukemia rat model: Parallels with human leukemogenesis.Animal models and experimental medicine · 2026Article
- SPINK2 silencing suppresses leukemic proliferation and restores myeloid commitment via MECOM downregulation in acute myeloid leukaemia.Cell death discovery · 2026Article
- Targeting dysregulated epigenetic and transcription factor networks inBlood neoplasia · 2026Article
- Myelodysplastic syndrome progress to acute myeloid leukemia: new insights and updates.Frontiers in immunology · 2026Review
- Article
- Chromatin accessibility in stem cells unveils progressive transcriptional alterations in myelodysplastic syndrome.Nature communications · 2025Article
- How to drug a leukemic stem cell: deciphering heterogeneity for better specificity.Blood neoplasia · 2025Review
- Retinoic acid and ascorbate synergize to suppress myeloid leukemia via TET2 activation.Cell reports · 2025Article
- Review
- Integrating multi-omics approaches in acute myeloid leukemia (AML): Advancements and clinical implications.Clinical and experimental medicine · 2025Review
71 more citing papers are in PubMed but not listed here.
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Authors and funding
24 authors at 9 institutions in 2 countries.
Funding
Abstract
Acute myeloid leukemia (AML) is a heterogeneous disease caused by a variety of alterations in transcription factors, epigenetic regulators and signaling molecules. To determine how different mutant regulators establish AML subtype-specific transcriptional networks, we performed a comprehensive global analysis of cis-regulatory element activity and interaction, transcription factor occupancy and gene expression patterns in purified leukemic blast cells. Here, we focused on specific subgroups of subjects carrying mutations in genes encoding transcription factors (RUNX1, CEBPα), signaling molecules (FTL3-ITD, RAS) and the nuclear protein NPM1). Integrated analysis of these data demonstrates that each mutant regulator establishes a specific transcriptional and signaling network unrelated to that seen in normal cells, sustaining the expression of unique sets of genes required for AML growth and maintenance.
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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.