ArticleLeukemia2014
Enhancers of Polycomb EPC1 and EPC2 sustain the oncogenic potential of MLL leukemia stem cells.
Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
The trial behind it
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
29 citing papers in PubMed, 44 citations in OpenAlex.
- Selective small molecule targeting of KDM4 as a therapeutic strategy to reduce proliferation of acute myeloid leukaemia.British journal of haematology · 2026Article
- Mammalian H4K16ac regulates the spatiotemporal order of genome replication rather than gene expression.Nucleic acids research · 2025Article
- Evaluation of the Circadian Rhythm Component Cipc (Clock-Interacting Pacemaker) in Leukemogenesis: A Literature Review and Bioinformatics Approach.Clocks & sleep · 2025Review
- Review
- EPC1/2 regulate hematopoietic stem and progenitor cell proliferation by modulating H3 acetylation and DLST.iScience · 2024Article
- Unconventional roles of chromatin remodelers and long non-coding RNAs in cell division.Cellular and molecular life sciences : CMLS · 2023Review
- Properties of Leukemic Stem Cells in Regulating Drug Resistance in Acute and Chronic Myeloid Leukemias.Biomedicines · 2022Review
- Identification and characterization of relapse-initiating cells in MLL-rearranged infant ALL by single-cell transcriptomics.Leukemia · 2022Article
- Article
- Blast cells surviving acute myeloid leukemia induction therapy are in cycle with a signature of FOXM1 activity.BMC cancer · 2021Article
- Enhancer recruitment of transcription repressors RUNX1 and TLE3 by mis-expressed FOXC1 blocks differentiation in acute myeloid leukemia.Cell reports · 2021Article
- Fusion genes in gynecologic tumors: the occurrence, molecular mechanism and prospect for therapy.Cell death & disease · 2021Review
- Inhibition of YTHDF2 triggers proteotoxic cell death in MYC-driven breast cancer.Molecular cell · 2021Article
- A genetic screen in Drosophila uncovers the multifaceted properties of the NUP98-HOXA9 oncogene.PLoS genetics · 2021Article
- A KDM4A-PAF1-mediated epigenomic network is essential for acute myeloid leukemia cell self-renewal and survival.Cell death & disease · 2021Article
- Article
- RNA isoform screens uncover the essentiality and tumor-suppressor activity of ultraconserved poison exons.Nature genetics · 2020Article
- Identification of anOncotarget · 2018Article
- Critical genomic regulation mediated by Enhancer of Polycomb.Current genetics · 2018Review
- Transient and permanent changes in DNA methylation patterns in inorganic arsenic-mediated epithelial-to-mesenchymal transition.Toxicology and applied pharmacology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Through a targeted knockdown (KD) screen of chromatin regulatory genes, we identified the EP400 complex components EPC1 and EPC2 as critical oncogenic cofactors in acute myeloid leukemia (AML). EPC1 and EPC2 were required for the clonogenic potential of human AML cells of multiple molecular subtypes. Focusing on MLL-mutated AML as an exemplar, Epc1 or Epc2 KD-induced apoptosis of murine MLL-AF9 AML cells and abolished leukemia stem cell potential. By contrast, normal hematopoietic stem and progenitor cells (HSPC) were spared. Similar selectivity was observed for human primary AML cells versus normal CD34(+) HSPC. In keeping with these distinct functional consequences, Epc1 or Epc2 KD-induced divergent transcriptional consequences in murine MLL-AF9 granulocyte-macrophage progenitor-like (GMP) cells versus normal GMP, with a signature of increased MYC activity in leukemic but not normal cells. This was caused by accumulation of MYC protein and was also observed following KD of other EP400 complex genes. Pharmacological inhibition of MYC:MAX dimerization, or concomitant MYC KD, reduced apoptosis following EPC1 KD, linking the accumulation of MYC to cell death. Therefore, EPC1 and EPC2 are components of a complex that directly or indirectly serves to prevent MYC accumulation and AML cell apoptosis, thus sustaining oncogenic potential.
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What OpenQuestion holds
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.