ArticleBlood2019
RUNX1-targeted therapy for AML expressing somatic or germline mutation in RUNX1.
Article in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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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
65 citing papers in PubMed, 97 citations in OpenAlex.
- RUNX1-regulated ITGB1-enriched extracellular vesicles drive pancreatic cancer liver metastasis via fibrotic pre-metastatic niche formation.Journal of translational medicine · 2026Article
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- The METTL3-YTHDC1 axis mediates architectural RNA mMolecular cancer · 2025Article
- Omacetaxine and venetoclax in relapsed/refractory acute myeloid leukemia or myelodysplastic syndrome with mutant RUNX1.Blood neoplasia · 2025Article
- Unlocking biological insights from differentially expressed genes: Concepts, methods, and future perspectives.Journal of advanced research · 2025Review
- Defining heterogeneity in core regulatory circuitry reveals HOXB3 condensation as a potential target in glioblastoma.Nature cell biology · 2025Article
- Article
- Molecular Mechanisms of Biochanin A in AML Cells: Apoptosis Induction and Pathway-Specific Regulation in U937 and THP-1.International journal of molecular sciences · 2025Article
- JMJD1C forms condensate to facilitate a RUNX1-dependent gene expression program shared by multiple types of AML cells.Protein & cell · 2025Article
- Discovery of candidate functional non-coding mutations in acute myeloid leukemia using single-cell chromatin accessibility sequencing.Communications biology · 2025Article
- Core transcriptional regulatory circuitry molecule ZNF217 promotes AML cell proliferation by up-regulating MYB.International journal of biological sciences · 2025Article
- Super-enhancer omics in stem cell.Molecular cancer · 2024Review
- The role of RUNX1/NF-κB in regulating PVAT inflammation in aortic dissection.Scientific reports · 2024Article
- Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression.Leukemia · 2024Article
- Efficacy of novel agents against cellular models of familial platelet disorder with myeloid malignancy (FPD-MM).Blood cancer journal · 2024Article
- Article
- mEpigenetics · 2023Article
- 8-Hydroxydaidzein Induces Apoptosis and Inhibits AML-Associated Gene Expression in U-937 Cells: Potential Phytochemical for AML Treatment.Biomolecules · 2023Article
- DNA methylation-based subtypes of acute myeloid leukemia with distinct prognosis and clinical features.Clinical and experimental medicine · 2023Article
- SEanalysis 2.0: a comprehensive super-enhancer regulatory network analysis tool for human and mouse.Nucleic acids research · 2023Article
5 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
20 authors at 5 institutions in 2 countries.
Funding
Abstract
RUNX1 transcription factor regulates normal and malignant hematopoiesis. Somatic or germline mutant RUNX1 (mtRUNX1) is associated with poorer outcome in acute myeloid leukemia (AML). Knockdown or inhibition of RUNX1 induced more apoptosis of AML expressing mtRUNX1 versus wild-type RUNX1 and improved survival of mice engrafted with mtRUNX1-expressing AML. CRISPR/Cas9-mediated editing-out of RUNX1 enhancer (eR1) within its intragenic super-enhancer, or BET protein BRD4 depletion by short hairpin RNA, repressed RUNX1, inhibited cell growth, and induced cell lethality in AML cells expressing mtRUNX1. Moreover, treatment with BET protein inhibitor or degrader (BET-proteolysis targeting chimera) repressed RUNX1 and its targets, inducing apoptosis and improving survival of mice engrafted with AML expressing mtRUNX1. Library of Integrated Network-based Cellular Signatures 1000-connectivity mapping data sets queried with messenger RNA signature of RUNX1 knockdown identified novel expression-mimickers (EMs), which repressed RUNX1 and exerted in vitro and in vivo efficacy against AML cells expressing mtRUNX1. In addition, the EMs cinobufagin, anisomycin, and narciclasine induced more lethality in hematopoietic progenitor cells (HPCs) expressing germline mtRUNX1 from patients with AML compared with HPCs from patients with familial platelet disorder (FPD), or normal untransformed HPCs. These findings highlight novel therapeutic agents for AML expressing somatic or germline mtRUNX1.
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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.