ArticleTheranostics2021
Small-molecule inhibitor of AF9/ENL-DOT1L/AF4/AFF4 interactions suppresses malignant gene expression and tumor growth.
Article in Theranostics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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
23 citing papers in PubMed, 36 citations in OpenAlex.
- Review
- Epigenetic modifications in cancer drug resistance: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Mechanism of AF9 (MLLT3)-Partner Dissociation in Mixed-Lineage Leukemia-Rearranged Leukemia.JACS Au · 2026Article
- RBM15B recognizes H3K79me2 to guide selective mThe EMBO journal · 2026Article
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- Targeting protein disorder: the next hurdle in drug discovery.Nature reviews. Drug discovery · 2025Review
- 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
- Epigenetic therapies targeting histone lysine methylation: complex mechanisms and clinical challenges.The Journal of clinical investigation · 2024Review
- Rational design of small-sized peptidomimetic inhibitors disrupting protein-protein interaction.RSC medicinal chemistry · 2024Review
- Structural studies of intrinsically disordered MLL-fusion protein AF9 in complex with peptidomimetic inhibitors.Protein science : a publication of the Protein Society · 2024Article
- Telomerase Inhibition in the Treatment of Leukemia: A Comprehensive Review.Antioxidants (Basel, Switzerland) · 2024Review
- The disruptor of telomeric silencing 1-like (DOT1L) promotes peritoneal fibrosis through the upregulation and activation of protein tyrosine kinases.Molecular biomedicine · 2024Article
- The Biological Significance of AFF4: Promoting Transcription Elongation, Osteogenic Differentiation and Tumor Progression.Combinatorial chemistry & high throughput screening · 2024Review
- Article
- The human leukemic oncogene MLL-AF4 promotes hyperplastic growth of hematopoietic tissues iniScience · 2023Article
- Quinazolinone Compounds Have Potent Antiviral Activity against Zika and Dengue Virus.Journal of medicinal chemistry · 2023Article
- Novel insights into histone lysine methyltransferases in cancer therapy: From epigenetic regulation to selective drugs.Journal of pharmaceutical analysis · 2023Review
- Gene signature of m6A-related targets to predict prognosis and immunotherapy response in ovarian cancer.Journal of cancer research and clinical oncology · 2023Article
- Advances in molecular characterization of pediatric acute megakaryoblastic leukemia not associated with Down syndrome; impact on therapy development.Frontiers in cell and developmental biology · 2023Review
- Structure-activity relationship and antitumor activity of 1,4-pyrazine-containing inhibitors of histone acetyltransferases P300/CBP.European journal of medicinal chemistry · 2022Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Chromosome translocations involving mixed lineage leukemia (MLL) gene cause acute leukemia with a poor prognosis. MLL is frequently fused with transcription cofactors AF4 (~35%), AF9 (25%) or its paralog ENL (10%). The AHD domain of AF9/ENL binds to AF4, its paralog AFF4, or histone-H3 lysine-79 (H3K79) methyltransferase DOT1L. Formation of AF9/ENL/AF4/AFF4-containing super elongation complexes (SEC) and the catalytic activity of DOT1L are essential for MLL-rearranged leukemia. Protein-protein interactions (PPI) between AF9/ENL and DOT1L/AF4/AFF4 are therefore a potential drug target.
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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.