ArticleJournal of hematology & oncology2022
A proteolysis-targeting chimera molecule selectively degrades ENL and inhibits malignant gene expression and tumor growth.
Article in Journal of hematology & oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 30 citations in OpenAlex.
- Review
- Disrupting a Convergent Acetylation Circuit Collapses Leukemic Identity Across AML Subtypes.bioRxiv : the preprint server for biology · 2026Article
- Discovery of a Highly Potent and Selective ENL Degrader.Journal of medicinal chemistry · 2026Article
- Epigenetic modifications in cancer drug resistance: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Review
- A chemical-genetic interaction between PAF1 and ENL/AF9 YEATS inhibition.RSC chemical biology · 2026Article
- Next-Generation Proteolysis-Targeting Chimeras in Precision Oncology: Multifunctional Designs, Emerging Modalities, and Translational Prospects in Targeted Protein Degradation.Drug development research · 2025Review
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- Review
- Synthesis, Structure-Activity Relationships, and Antitumor Activities of Quinoxiline-Containing Inhibitors of the Protein-Protein Interactions between Transcription Coactivator AF9/ENL and DOT1L/AF4.Journal of medicinal chemistry · 2025Article
- Development of Chemical Tools for the Human YEATS Domain.ACS chemical biology · 2025Review
- Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024Review
- Characteristic roadmap of linker governs the rational design of PROTACs.Acta pharmaceutica Sinica. B · 2024Review
- A potent and selective ENL degrader suppresses oncogenic gene expression and leukemia progression.Science advances · 2024Article
- Pharmacological targeting of the cancer epigenome.Nature cancer · 2024Review
- Potential New Therapies "ROS-Based" in CLL: An Innovative Paradigm in the Induction of Tumor Cell Apoptosis.Antioxidants (Basel, Switzerland) · 2024Review
- Telomerase Inhibition in the Treatment of Leukemia: A Comprehensive Review.Antioxidants (Basel, Switzerland) · 2024Review
- Ferroptosis-Related lncRNA to Predict the Clinical Outcomes and Molecular Characteristics of Kidney Renal Papillary Cell Carcinoma.Current issues in molecular biology · 2024Article
- Overview of epigenetic degraders based on PROTAC, molecular glue, and hydrophobic tagging technologies.Acta pharmaceutica Sinica. B · 2024Review
- Small-molecule tools for YEATS domain proteins.Current opinion in chemical biology · 2023Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundChromosome translocations involving mixed lineage leukemia 1 (MLL1) cause acute leukemia in most infants and 5-10% children/adults with dismal clinical outcomes. Most frequent MLL1-fusion partners AF4/AFF4, AF9/ENL and ELL, together with CDK9/cyclin-T1, constitute super elongation complexes (SEC), which promote aberrant gene transcription, oncogenesis and maintenance of MLL1-rearranged (MLL1-r) leukemia. Notably, ENL, but not its paralog AF9, is essential for MLL1-r leukemia (and several other cancers) and therefore a drug target. Moreover, recurrent ENL mutations are found in Wilms tumor, the most common pediatric kidney cancer, and play critical roles in oncogenesis.
methodsProteolysis-Targeting Chimera (PROTAC) molecules were designed and synthesized to degrade ENL. Biological activities of these compounds were characterized in cell and mouse models of MLL1-r leukemia and other cancers.
resultsCompound 1 efficiently degraded ENL with DC
conclusionCompound 1 is a novel chemical probe for cellular and in vivo studies of ENL (including its oncogenic mutants) and a lead compound for further anticancer drug development.
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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.