ArticleOncotarget2018
Multi-omics profiling reveals a distinctive epigenome signature for high-risk acute promyelocytic leukemia.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Comprehensive lincRNA Transcriptome in Acute Myeloid Leukemia: Integrating Known and Newly Identified lincRNAs Across Pediatric and Adult Cohorts.Non-coding RNA · 2026Article
- Breaking the Bone Marrow Barrier: Peripheral Blood as a Gateway to Measurable Residual Disease Detection in Acute Myelogenous Leukemia.American journal of hematology · 2025Review
- In vivo temporal resolution of acute promyelocytic leukemia progression reveals a role ofGenes & development · 2022Article
- MLL5 improves ATRA driven differentiation and promotes xenotransplant engraftment in acute promyelocytic leukemia model.Cell death & disease · 2021Article
- Roles of Histone Deacetylases in Acute Myeloid Leukemia With Fusion Proteins.Frontiers in oncology · 2021Review
- Reduced SLIT2 is Associated with Increased Cell Proliferation and Arsenic Trioxide Resistance in Acute Promyelocytic Leukemia.Cancers · 2020Article
- Properly Substituted Cyclic Bis-(2-bromobenzylidene) Compounds Behaved as Dual p300/CARM1 Inhibitors and Induced Apoptosis in Cancer Cells.Molecules (Basel, Switzerland) · 2020Article
- Epigenetic Modifications in Acute Myeloid Leukemia: Prognosis, Treatment, and Heterogeneity.Frontiers in genetics · 2019Review
Corrections and comments
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Authors and funding
31 authors.
Funding
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Abstract
Epigenomic alterations have been associated with both pathogenesis and progression of cancer. Here, we analyzed the epigenome of two high-risk APL (hrAPL) patients and compared it to non-high-risk APL cases. Despite the lack of common genetic signatures, we found that human hrAPL blasts from patients with extremely poor prognosis display specific patterns of histone H3 acetylation, specifically hyperacetylation at a common set of enhancer regions. In addition, unique profiles of the repressive marks H3K27me3 and DNA methylation were exposed in high-risk APLs. Epigenetic comparison with low/intermediate-risk APLs and AMLs revealed hrAPL-specific patterns of histone acetylation and DNA methylation, suggesting these could be further developed into markers for clinical identification. The epigenetic drug MC2884, a newly generated general HAT/EZH2 inhibitor, induces apoptosis of high-risk APL blasts and reshapes their epigenomes by targeting both active and repressive marks. Together, our analysis uncovers distinctive epigenome signatures of hrAPL patients, and provides proof of concept for use of epigenome profiling coupled to epigenetic drugs to 'personalize' precision medicine.
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