ArticleCell reports2013
RUNX1 is a key target in t(4;11) leukemias that contributes to gene activation through an AF4-MLL complex interaction.
Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
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Who cites it
92 citing papers in PubMed, 148 citations in OpenAlex.
- 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
- Multiomic single cell sequencing identifies stemlike nature of mixed phenotype acute leukemia.Nature communications · 2024Article
- Sequential drug treatment targeting cell cycle and cell fate regulatory programs blocks non-genetic cancer evolution in acute lymphoblastic leukemia.Genome biology · 2024Article
- Functional relevance of circRNA aberrant expression in pediatric acute leukemia with KMT2A::AFF1 fusion.Blood advances · 2024Article
- Targeting IGF2BP3 enhances antileukemic effects of menin-MLL inhibition in MLL-AF4 leukemia.Blood advances · 2024Article
- CRISPR-Cas9 Library Screening Identifies Novel Molecular Vulnerabilities inInternational journal of molecular sciences · 2023Article
- RUNX1 mutation has no prognostic significance in paediatric AML: a retrospective study of the AML-BFM study group.Leukemia · 2023Article
- Choosing the Right Cell Line for Acute Myeloid Leukemia (AML) Research.International journal of molecular sciences · 2023Review
- The ENL YEATS epigenetic reader domain critically links MLL-ENL to leukemic stem cell frequency in t(11;19) Leukemia.Leukemia · 2023Article
- Regulome analysis in B-acute lymphoblastic leukemia exposes Core Binding Factor addiction as a therapeutic vulnerability.Nature communications · 2022Article
- HigherEJHaem · 2022Article
- Article
- MiR-27a downregulates 14-3-3θ, RUNX1, AF4, and MLL-AF4, crucial drivers of blast transformation in t(4;11) leukemia cells.Cell biochemistry and function · 2022Article
- In vivo genome-wide CRISPR screening in murine acute myeloid leukemia uncovers microenvironmental dependencies.Blood advances · 2022Article
- SMGR: a joint statistical method for integrative analysis of single-cell multi-omics data.NAR genomics and bioinformatics · 2022Article
- Article
- Effective tumor cell abrogation via Venetoclax-mediated BCL-2 inhibition in KMT2A-rearranged acute B-lymphoblastic leukemia.Cell death discovery · 2022Article
- IKAROS and MENIN coordinate therapeutically actionable leukemogenic gene expression in MLL-r acute myeloid leukemia.Nature cancer · 2022Article
- Defining the fetal origin of MLL-AF4 infant leukemia highlights specific fatty acid requirements.Cell reports · 2021Article
32 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
The Mixed Lineage Leukemia (MLL) protein is an important epigenetic regulator required for the maintenance of gene activation during development. MLL chromosomal translocations produce novel fusion proteins that cause aggressive leukemias in humans. Individual MLL fusion proteins have distinct leukemic phenotypes even when expressed in the same cell type, but how this distinction is delineated on a molecular level is poorly understood. Here, we highlight a unique molecular mechanism whereby the RUNX1 gene is directly activated by MLL-AF4 and the RUNX1 protein interacts with the product of the reciprocal AF4-MLL translocation. These results support a mechanism of transformation whereby two oncogenic fusion proteins cooperate by activating a target gene and then modulating the function of its downstream product.
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