ArticleLeukemia2013
Increased anti-leukemic activity of decitabine via AR-42-induced upregulation of miR-29b: a novel epigenetic-targeting approach in acute myeloid leukemia.
Article in Leukemia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02698124 (Prospective Observation of the indUction Regimen for Acute Non-Promyelocytic Myeloid Leukemia in Elderly; Decitabine for Chemotherapy Unfit Korean Acute Myeloid Leukemia), which is not on this map. Cited by 38 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.
Prospective Observation of the indUction Regimen for Acute Non-Promyelocytic Myeloid Leukemia in Elderly; Decitabine for Chemotherapy Unfit Korean Acute Myeloid Leukemia (AML) Patients in Real Practice
Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- Decitabine induces cell differentiation and growth inhibition accompanied by upregulation of microRNA-143 and MS4A3 in the myelodysplastic syndromes-derived leukemic cell line MDS-L.Oncology letters · 2026Article
- HDAC inhibitors in cancer therapy: sensitization mechanisms, combination strategies, and translational challenges.Frontiers in cell and developmental biology · 2026Review
- The miRNA Landscape of Leukemia - Cellular Actions to Therapy through Molecular Mechanisms.Cell biochemistry and biophysics · 2025Review
- The epigenetic revolution in hematology: from benchside breakthroughs to clinical transformations.Clinical and experimental medicine · 2025Review
- The Role of the DNA Methyltransferase Family and the Therapeutic Potential of DNMT Inhibitors in Tumor Treatment.Current oncology (Toronto, Ont.) · 2025Review
- Epigenetic mechanisms of drug resistance in acute myeloid leukemia: advances in small-molecule targeted therapy.Frontiers in pharmacology · 2025Review
- A phase 1 trial of the histone deacetylase inhibitor AR-42 in patients with neurofibromatosis type 2-associated tumors and advanced solid malignancies.Cancer chemotherapy and pharmacology · 2021Article
- Targeting DNA Damage Repair Functions of Two Histone Deacetylases, HDAC8 and SIRT6, Sensitizes Acute Myeloid Leukemia to NAMPT Inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Clinical Applications of MicroRNAs in Acute Myeloid Leukemia: A Mini-Review.Frontiers in oncology · 2021Review
- Chidamide acts on the histone deacetylase-mediated miR-34a/Bcl-2 axis to regulate NB4 cell line proliferation and apoptosis.The Kaohsiung journal of medical sciences · 2020Article
- Phase I study of AR-42 and decitabine in acute myeloid leukemia.Leukemia & lymphoma · 2020Article
- Decitabine shows anti-acute myeloid leukemia potential via regulating the miR-212-5p/CCNT2 axis.Open life sciences · 2020Article
- MicroRNAs Associated With a Good Prognosis of Acute Myeloid Leukemia and Their Effect on Macrophage Polarization.Frontiers in immunology · 2020Review
- Small Molecules Targeting HATs, HDACs, and BRDs in Cancer Therapy.Frontiers in oncology · 2020Review
- Long non-coding RNA SNHG1 indicates poor prognosis and facilitates disease progression in acute myeloid leukemia.Biology open · 2019Article
- Oncogenic Roles and Inhibitors of DNMT1, DNMT3A, and DNMT3B in Acute Myeloid Leukaemia.Biomarker insights · 2019Review
- Hypomethylating Agents as a Therapy for AML.Current hematologic malignancy reports · 2017Review
- Therapeutic Resistance in Acute Myeloid Leukemia: The Role of Non-Coding RNAs.International journal of molecular sciences · 2016Review
- Article
- Midostaurin, bortezomib and MEC in relapsed/refractory acute myeloid leukemia.Leukemia & lymphoma · 2016Article
Corrections and comments
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Authors and funding
24 authors at 1 institution in 1 country.
Funding
Abstract
Histone deacetylase (HDAC) inhibitors either alone or in combination with hypomethylating agents have limited clinical effect in acute myeloid leukemia (AML). Previously, we demonstrated that AML patients with higher miR (microRNA)-29b expression had better response to the hypomethylating agent decitabine. Therefore, an increase in miR-29b expression preceding decitabine treatment may provide a therapeutic advantage. We previously showed that miR-29b expression is suppressed by a repressor complex that includes HDACs. Thus, HDAC inhibition may increase miR-29b expression. We hypothesized that priming AML cells with the novel HDAC inhibitor (HDACI) AR-42 would result in increased response to decitabine treatment via upregulation of miR-29b. Here, we show that AR-42 is a potent HDACI in AML, increasing miR-29b levels and leading to downregulation of known miR-29b targets (that is, SP1, DNMT1, DNMT3A and DNMT3B). We then demonstrated that the sequential administration of AR-42 followed by decitabine resulted in a stronger anti-leukemic activity in vitro and in vivo than decitabine followed by AR-42 or either drug alone. These preclinical results with AR-42 priming before decitabine administration represent a promising, novel treatment approach and a paradigm shift with regard to the combination of epigenetic-targeting compounds in AML, where decitabine has been traditionally given before HDACIs.
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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.