ArticleThe Journal of experimental medicine2017
RUNX1 cooperates with FLT3-ITD to induce leukemia.
Article in The Journal of experimental medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- RUNX1A isoform is overexpressed in acute myeloid leukemia and is associated with FLT3 internal tandem duplications.Cancer gene therapy · 2025Article
- Clinical significance of the transcription factor (SOX11) expression in the bone marrow of acute myeloid leukemia patients.World journal of clinical oncology · 2025Article
- Activating mutations remodel the chromatin accessibility landscape to drive distinct regulatory networks inHemaSphere · 2024Article
- Pharmacological inhibition of RAS overcomes FLT3 inhibitor resistance in FLT3-ITD+ AML through AP-1 and RUNX1.iScience · 2024Article
- Gene regulatory network analysis predicts cooperating transcription factor regulons required for FLT3-ITD+ AML growth.Cell reports · 2023Article
- The Haematopoietically-expressed homeobox transcription factor: roles in development, physiology and disease.Frontiers in immunology · 2023Review
- HigherEJHaem · 2022Article
- Evaluating the frequency, prognosis and survival of RUNX1 and ASXL1 mutations in patients with acute myeloid leukaemia in northeastern Iran.Journal of cellular and molecular medicine · 2022Article
- Review
- Loss of SIRT1 inhibits hematopoietic stem cell aging and age-dependent mixed phenotype acute leukemia.Communications biology · 2022Article
- Review
- Combinatorial molecule screening identified a novel diterpene and the BET inhibitor CPI-203 as differentiation inducers of primary acute myeloid leukemia cells.Haematologica · 2021Article
- SETBP1 overexpression acts in the place of class-defining mutations to drive FLT3-ITD-mutant AML.Blood advances · 2021Article
- Immunopeptidogenomics: Harnessing RNA-Seq to Illuminate the Dark Immunopeptidome.Molecular & cellular proteomics : MCP · 2021Article
- Studying leukemia stem cell properties and vulnerabilities with human iPSCs.Stem cell research · 2021Article
- Review
- RUNX1: an emerging therapeutic target for cardiovascular disease.Cardiovascular research · 2020Review
- RUNX1 Dosage in Development and Cancer.Molecules and cells · 2020Review
- Identification of the hub genes RUNX2 and FN1 in gastric cancer.Open medicine (Warsaw, Poland) · 2020Article
- Distinct association of RUNX family expression with genetic alterations and clinical outcome in acute myeloid leukemia.Cancer biomarkers : section A of Disease markers · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is induced by the cooperative action of deregulated genes that perturb self-renewal, proliferation, and differentiation. Internal tandem duplications (ITDs) in the FLT3 receptor tyrosine kinase are common mutations in AML, confer poor prognosis, and stimulate myeloproliferation. AML patient samples with FLT3-ITD express high levels of RUNX1, a transcription factor with known tumor-suppressor function. In this study, to understand this paradox, we investigated the impact of RUNX1 and FLT3-ITD coexpression. FLT3-ITD directly impacts on RUNX1 activity, whereby up-regulated and phosphorylated RUNX1 cooperates with FLT3-ITD to induce AML. Inactivating RUNX1 in tumors releases the differentiation block and down-regulates genes controlling ribosome biogenesis. We identified
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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.