ArticleExperimental hematology2017
MLL-AF4 binds directly to a BCL-2 specific enhancer and modulates H3K27 acetylation.
Article in Experimental hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- BCL-2 and MCL1 co-inhibition enhances glucocorticoid therapy in preclinical models of infant KMT2A-rearranged acute lymphoblastic leukaemia.British journal of haematology · 2026Article
- Emerging genomic biomarkers in diagnosis and classification of T-cell acute lymphoblastic leukemia.Hematology. American Society of Hematology. Education Program · 2025Review
- Suppressing t(4;11) Acute Leukemia by Lipopolymer Nanoparticle Delivery of siRNA Targeting KMT2A::AFF1 with Enhanced Extrahepatic Delivery.Advanced healthcare materials · 2025Article
- The Inositol-5-Phosphatase SHIP1: Expression, Regulation and Role in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2025Review
- Chemotherapy-free treatment of B-lymphoid/myeloid mixed phenotype acute leukemia: two case reports and literature review.Immunotherapy · 2025Review
- Lessons learned from 20 years of preclinical testing in pediatric cancers.Pharmacology & therapeutics · 2024Review
- Venetoclax in combination with chidamide and azacitidine for the treatment of relapsed/refractory B-cell acute lymphoblastic leukemia with theFrontiers in immunology · 2024Review
- MLL-AF4 cooperates with PAF1 and FACT to drive high-density enhancer interactions in leukemia.Nature communications · 2023Article
- 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
- Defining the fetal origin of MLL-AF4 infant leukemia highlights specific fatty acid requirements.Cell reports · 2021Article
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- Review
- Emerging molecular subtypes and therapeutic targets in B-cell precursor acute lymphoblastic leukemia.Frontiers of medicine · 2021Review
- Nuclear FGFR2 Interacts with the MLL-AF4 Oncogenic Chimera and Positively RegulatesInternational journal of molecular sciences · 2021Article
- Epigenetic Control of Infant B Cell Precursor Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2021Review
- BET inhibition disrupts transcription but retains enhancer-promoter contact.Nature communications · 2021Article
- Functional interrogation of HOXA9 regulome in MLLr leukemia via reporter-based CRISPR/Cas9 screen.eLife · 2020Article
- CDKI-73: an orally bioavailable and highly efficacious CDK9 inhibitor against acute myeloid leukemia.Investigational new drugs · 2019Article
- DOT1L inhibition reveals a distinct subset of enhancers dependent on H3K79 methylation.Nature communications · 2019Article
- SRPK1 maintains acute myeloid leukemia through effects on isoform usage of epigenetic regulators including BRD4.Nature communications · 2018Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Survival rates for children and adults carrying mutations in the Mixed Lineage Leukemia (MLL) gene continue to have a very poor prognosis. The most common MLL mutation in acute lymphoblastic leukemia is the t(4;11)(q21;q23) chromosome translocation that fuses MLL in-frame with the AF4 gene producing MLL-AF4 and AF4-MLL fusion proteins. Previously, we found that MLL-AF4 binds to the BCL-2 gene and directly activates it through DOT1L recruitment and increased H3K79me2/3 levels. In the study described here, we performed a detailed analysis of MLL-AF4 regulation of the entire BCL-2 family. By measuring nascent RNA production in MLL-AF4 knockdowns, we found that of all the BCL-2 family genes, MLL-AF4 directly controls the active transcription of both BCL-2 and MCL-1 and also represses BIM via binding of the polycomb group repressor 1 (PRC1) complex component CBX8. We further analyzed MLL-AF4 activation of the BCL-2 gene using Capture-C and identified a BCL-2-specific enhancer, consisting of two clusters of H3K27Ac at the 3' end of the gene. Loss of MLL-AF4 activity results in a reduction of H3K79me3 levels in the gene body and H3K27Ac levels at the 3' BCL-2 enhancer, revealing a novel regulatory link between these two histone marks and MLL-AF4-mediated activation of BCL-2.
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