ArticleThe Journal of clinical investigation2013
Transcription factor RUNX1 promotes survival of acute myeloid leukemia cells.
Article in The Journal of clinical investigation, 2013. 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 128 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
128 citing papers in PubMed, 195 citations in OpenAlex.
- RUNX1 upregulation and RUNX1-ETO depletion inhibits survival of t(8;21)-positive leukemia cells.Global medical genetics · 2026Article
- Co-option of lineage plasticity as a hallmark of multipotent acute leukemias.Blood neoplasia · 2026Review
- Inhibition of adipocyte RUNX1/2 enhances adipose tissue thermogenesis through distinct mechanisms.Nature communications · 2026Article
- Insights from pooled CRISPRi single-cell screens in K562 cells reveal gene functions, regulatory networks, and highlight opportunities and limitations.BMC genomics · 2026Article
- VHL synthetic lethality screens uncover CBF-β as a negative regulator of STING.Nature communications · 2026Article
- The METTL3-YTHDC1 axis mediates architectural RNA mMolecular cancer · 2025Article
- JMJD1C forms condensate to facilitate a RUNX1-dependent gene expression program shared by multiple types of AML cells.Protein & cell · 2025Article
- Nanoplastics: Immune Impact, Detection, and Internalization after Human Blood Exposure by Single-Cell Mass Cytometry.Advanced materials (Deerfield Beach, Fla.) · 2025Article
- Acute resistance to BET inhibitors remodels compensatory transcriptional programs via p300 coactivation.Blood · 2025Article
- Redistribution of PU.1 partner transcription factor RUNX1 binding secures cell survival during leukemogenesis.The EMBO journal · 2024Article
- Modeling and therapeutic targeting of t(8;21) AML with/without TP53 deficiency.International journal of hematology · 2024Article
- Interface-guided phenotyping of coding variants in the transcription factor RUNX1.Cell reports · 2024Article
- Simultaneous screening of overexpressed genes in breast cancer for oncogenic drivers and tumor dependencies.Scientific reports · 2024Article
- RUNX1 C-terminal mutations impair blood cell differentiation by perturbing specific enhancer-promoter networks.Blood advances · 2024Article
- Apoptosis-related prognostic biomarkers and potential targets for acute kidney injury based on machine learning algorithm and in vivo experiments.Apoptosis : an international journal on programmed cell death · 2024Article
- Article
- ELF4 was a prognostic biomarker and related to immune infiltrates in glioma.Journal of Cancer · 2024Article
- Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth.Cell reports · 2023Article
- Combination of RUNX1 inhibitor and gemcitabine mitigates chemo-resistance in pancreatic ductal adenocarcinoma by modulating BiP/PERK/eIF2α-axis-mediated endoplasmic reticulum stress.Journal of experimental & clinical cancer research : CR · 2023Article
- RUN(X) out of blood: emerging RUNX1 functions beyond hematopoiesis and links to Down syndrome.Human genomics · 2023Review
68 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
RUNX1 is generally considered a tumor suppressor in myeloid neoplasms. Inactivating RUNX1 mutations have frequently been found in patients with myelodysplastic syndrome (MDS) and cytogenetically normal acute myeloid leukemia (AML). However, no somatic RUNX1 alteration was found in AMLs with leukemogenic fusion proteins, such as core-binding factor (CBF) leukemia and MLL fusion leukemia, raising the possibility that RUNX1 could actually promote the growth of these leukemia cells. Using normal human cord blood cells and those expressing leukemogenic fusion proteins, we discovered a dual role of RUNX1 in myeloid leukemogenesis. RUNX1 overexpression inhibited the growth of normal cord blood cells by inducing myeloid differentiation, whereas a certain level of RUNX1 activity was required for the growth of AML1-ETO and MLL-AF9 cells. Using a mouse genetic model, we also showed that the combined loss of Runx1/Cbfb inhibited leukemia development induced by MLL-AF9. RUNX2 could compensate for the loss of RUNX1. The survival effect of RUNX1 was mediated by BCL2 in MLL fusion leukemia. Our study unveiled an unexpected prosurvival role for RUNX1 in myeloid leukemogenesis. Inhibiting RUNX1 activity rather than enhancing it could be a promising therapeutic strategy for AMLs with leukemogenic fusion proteins.
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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.