ArticleThe Journal of clinical investigation2016
PML-RARA requires DNA methyltransferase 3A to initiate acute promyelocytic leukemia.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Acute promyelocytic leukemia with a unique genetic signature: a case report and management.Discover oncology · 2026Article
- Hypomethylation ofFrontiers in immunology · 2025Article
- CD34 Protein: Its expression and function in inflammation.Cell and tissue research · 2023Review
- The PML hub: An emerging actor of leukemia therapies.The Journal of experimental medicine · 2023Article
- In vivo temporal resolution of acute promyelocytic leukemia progression reveals a role ofGenes & development · 2022Article
- Epigenetic modifications in acute myeloid leukemia: The emerging role of circular RNAs (Review).International journal of oncology · 2021Review
- Article
- Oncogenes, Proto-Oncogenes, and Lineage Restriction of Cancer Stem Cells.International journal of molecular sciences · 2021Review
- Dual functions of SPOP and ERG dictate androgen therapy responses in prostate cancer.Nature communications · 2021Article
- Kdm6a deficiency restricted to mouse hematopoietic cells causes an age- and sex-dependent myelodysplastic syndrome-like phenotype.PloS one · 2021Article
- Hypomethylating Agent Azacitidine Is Effective in Treating Brain Metastasis Triple-Negative Breast Cancer Through Regulation of DNA Methylation of Keratin 18 Gene.Translational oncology · 2020Article
- SERS-Based Assessment of MRD in Acute Promyelocytic Leukemia?Frontiers in oncology · 2020Review
- Lentiviral CRISPR/Cas9-Mediated Genome Editing for the Study of Hematopoietic Cells in Disease Models.Journal of visualized experiments : JoVE · 2019Article
- Aberrant DNA Methylation in Acute Myeloid Leukemia and Its Clinical Implications.International journal of molecular sciences · 2019Review
- Acute Promyelocytic Leukemia: A History over 60 Years-From the Most Malignant to the most Curable Form of Acute Leukemia.Oncology and therapy · 2019Review
- Overview of DNA Self-Assembling: Progresses in Biomedical Applications.Pharmaceutics · 2018Review
- Selected biological issues affecting relapse after stem cell transplantation: role of T-cell impairment, NK cells and intrinsic tumor resistance.Bone marrow transplantation · 2018Review
- PML Recruits TET2 to Regulate DNA Modification and Cell Proliferation in Response to Chemotherapeutic Agent.Cancer research · 2018Article
- Epigenetic heterogeneity affects the risk of relapse in children with t(8;21)RUNX1-RUNX1T1-rearranged AML.Leukemia · 2018Article
- Low HOX gene expression in PML-RARα-positive leukemia results from suppressed histone demethylation.Epigenetics · 2018Article
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Authors and funding
9 authors.
Funding
Abstract
The DNA methyltransferases DNMT3A and DNMT3B are primarily responsible for de novo methylation of specific cytosine residues in CpG dinucleotides during mammalian development. While loss-of-function mutations in DNMT3A are highly recurrent in acute myeloid leukemia (AML), DNMT3A mutations are almost never found in AML patients with translocations that create oncogenic fusion genes such as PML-RARA, RUNX1-RUNX1T1, and MLL-AF9. Here, we explored how DNMT3A is involved in the function of these fusion genes. We used retroviral vectors to express PML-RARA, RUNX1-RUNX1T1, or MLL-AF9 in bone marrow cells derived from WT or DNMT3A-deficient mice. Additionally, we examined the phenotypes of hematopoietic cells from Ctsg-PML-RARA mice, which express PML-RARA in early hematopoietic progenitors and myeloid precursors, with or without DNMT3A. We determined that the methyltransferase activity of DNMT3A, but not DNMT3B, is required for aberrant PML-RARA-driven self-renewal ex vivo and that DNMT3A is dispensable for RUNX1-RUNX1T1- and MLL-AF9-driven self-renewal. Furthermore, both the PML-RARA-driven competitive transplantation advantage and development of acute promyelocytic leukemia (APL) required DNMT3A. Together, these findings suggest that PML-RARA requires DNMT3A to initiate APL in mice.
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