ArticleCell2017
Therapeutic Targeting of MLL Degradation Pathways in MLL-Rearranged Leukemia.
Article in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
73 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.
- Nucleosome Turnover Regulates Histone Methylation Patterns over the Genome.Molecular cell · 2019Pooled it
- Promiscuous RNA binding by WDR5 remodels the KMT2A (MLL1) histone methyltransferase complex to an inactive state.Molecular cell · 2026Article
- Promiscuous RNA binding by WDR5 remodels the KMT2A (MLL1) histone methyltransferase complex to an inactive state.bioRxiv : the preprint server for biology · 2026Article
- Immune interplay between sepsis and haematological malignancies.Intensive care medicine experimental · 2026Review
- Chromatin-associated circRNA ciCRLF3(2) regulates cell differentiation blockage via activating non-homologous end joining-based DNA repair.Cell death and differentiation · 2026Article
- Fusion oncoproteins orchestrate tumorigenesis and sustain malignant progression via a positive feedback mechanism.Cell & bioscience · 2026Review
- Specificity protein 1 initiates epithelial-mesenchymal transition of circulating tumor cells to inhibit metastasis in prostate cancer.Cancer cell international · 2025Article
- Review
- Ectopic expression of testis-specific transcription elongation factor in driving cancer.Science advances · 2025Article
- The Ubiquitin-Conjugating Enzyme E2 O (UBE2O) and Its Therapeutic Potential in Human Leukemias and Solid Tumors.Cancers · 2024Review
- Blockade of the lncRNA-DOT1L-LAMP5 axis enhances autophagy and promotes degradation of MLL fusion proteins.Experimental hematology & oncology · 2024Article
- Article
- Article
- Menin-MLL1 Interaction Small Molecule Inhibitors: A Potential Therapeutic Strategy for Leukemia and Cancers.Molecules (Basel, Switzerland) · 2023Review
- IMPDH inhibition activates TLR-VCAM1 pathway and suppresses the development of MLL-fusion leukemia.EMBO molecular medicine · 2023Article
- Endogenous IL-1 receptor antagonist restricts healthy and malignant myeloproliferation.Nature communications · 2023Article
- UBE2O ubiquitinates PTRF/CAVIN1 and inhibits the secretion of exosome-related PTRF/CAVIN1.Cell communication and signaling : CCS · 2022Article
- Inflammatory bone marrow signaling in pediatric acute myeloid leukemia distinguishes patients with poor outcomes.Nature communications · 2022Article
- UBE2O promotes lipid metabolic reprogramming and liver cancer progression by mediating HADHA ubiquitination.Oncogene · 2022Article
- Interleukin-4 treatment reduces leukemia burden in acute myeloid leukemia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
Chromosomal translocations of the mixed-lineage leukemia (MLL) gene with various partner genes result in aggressive leukemia with dismal outcomes. Despite similar expression at the mRNA level from the wild-type and chimeric MLL alleles, the chimeric protein is more stable. We report that UBE2O functions in regulating the stability of wild-type MLL in response to interleukin-1 signaling. Targeting wild-type MLL degradation impedes MLL leukemia cell proliferation, and it downregulates a specific group of target genes of the MLL chimeras and their oncogenic cofactor, the super elongation complex. Pharmacologically inhibiting this pathway substantially delays progression, and it improves survival of murine leukemia through stabilizing wild-type MLL protein, which displaces the MLL chimera from some of its target genes and, therefore, relieves the cellular oncogenic addiction to MLL chimeras. Stabilization of MLL provides us with a paradigm in the development of therapies for aggressive MLL leukemia and perhaps for other cancers caused by translocations.
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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.