ArticleOncotarget2017
Comprehensive mapping of the effects of azacitidine on DNA methylation, repressive/permissive histone marks and gene expression in primary cells from patients with MDS and MDS-related disease.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 63 citations in OpenAlex.
- Transposable elements in hematopoietic stem cells upon aging and myeloid malignancies.Mobile DNA · 2026Review
- Integrated FHIT and IDH2 biomarker profiling predicts lethal sensitivity to DCPS inhibition in Acute Myeloid Leukemia and Myelodysplastic syndrome.Discover oncology · 2026Article
- p53 status determines the epigenetic response to demethylating agents azacitidine and decitabine.EMBO reports · 2026Article
- Parasitic Infections and Carcinogenesis: Molecular Mechanisms, Immune Modulation, and Emerging Therapeutic Strategies.Oncology research · 2026Review
- A bibliometric review of triazine hybrids: synthesis, reactions, and applications spanning the last quarter-century (2000-2025).RSC advances · 2025Review
- Advances and challenges in drug repurposing in precision therapeutics of colorectal cancer.World journal of gastrointestinal oncology · 2025Review
- Transcriptomic analysis of non-leukemic cell subsets in azacytidine-responsive AML highlights pathways associated with adhesion, platelet aggregation, and angiogenesis in mice and humans.Molecular medicine (Cambridge, Mass.) · 2025Article
- Assessment of chromatin remodeling of acute myeloid leukemia cells treated with gilteritinib: a case report.Journal of medical case reports · 2025Article
- Endogenous retroelements in hematological malignancies: From epigenetic dysregulation to therapeutic targeting.American journal of hematology · 2025Review
- Effects of Hypomethylating Agents on Gene Modulation in the Leukemic Microenvironment and Disease Trajectory in a Mouse Model of AML.bioRxiv : the preprint server for biology · 2024Article
- Targeting heterochromatin eliminates chronic myelomonocytic leukemia malignant stem cells through reactivation of retroelements and immune pathways.Communications biology · 2024Article
- Epigenetic Modeling of Jumping Translocations of 1q Heterochromatin in Acute Myeloid Leukemia After 5'-Azacytidine Treatment.Genes, chromosomes & cancer · 2024Article
- Transcripts of repetitive DNA elements signal to block phagocytosis of hematopoietic stem cells.Science (New York, N.Y.) · 2024Article
- Article
- UHRF1/DNMT1-MZF1 axis-modulated intragenic site-specific CpGI methylation confers divergent expression and opposing functions ofActa pharmaceutica Sinica. B · 2023Article
- Genome-wide analysis toward the epigenetic aetiology of myelodysplastic syndrome disease progression and pharmacoepigenomic basis of hypomethylating agents drug treatment response.Human genomics · 2023Article
- Clinical advances in epigenetic therapies for lymphoma.Clinical epigenetics · 2023Review
- Determination of 5-azacitidine in human plasma by LC-MS/MS: application to pharmacokinetics pilot study in MDS/AML patients.Cancer chemotherapy and pharmacology · 2023Article
- 5-azacytidine inhibits Sox2 promoter methylation during the induction of Thy-1American journal of translational research · 2023Article
- HERVs characterize normal and leukemia stem cells and represent a source of shared epitopes for cancer immunotherapy.American journal of hematology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Azacitidine (Aza) is first-line treatment for patients with high-risk myelodysplastic syndromes (MDS), although its precise mechanism of action is unknown. We performed the first study to globally evaluate the epigenetic effects of Aza on MDS bone marrow progenitor cells assessing gene expression (RNA seq), DNA methylation (Illumina 450k) and the histone modifications H3K18ac and H3K9me3 (ChIP seq). Aza induced a general increase in gene expression with 924 significantly upregulated genes but this increase showed no correlation with changes in DNA methylation or H3K18ac, and only a weak association with changes in H3K9me3. Interestingly, we observed activation of transcripts containing 15 endogenous retroviruses (ERVs) confirming previous cell line studies. DNA methylation decreased moderately in 99% of all genes, with a median β-value reduction of 0.018; the most pronounced effects seen in heterochromatin. Aza-induced hypomethylation correlated significantly with change in H3K9me3. The pattern of H3K18ac and H3K9me3 displayed large differences between patients and healthy controls without any consistent pattern induced by Aza. We conclude that the marked induction of gene expression only partly could be explained by epigenetic changes, and propose that activation of ERVs may contribute to the clinical effects of Aza in MDS.
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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.