ReviewAdvances in therapy2022
The Clinical Value of Decitabine Monotherapy in Patients with Acute Myeloid Leukemia.
Review in Advances in therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Midostaurin plus daunorubicin or idarubicin for young and older adults with FLT3-mutated AML: a phase 3b trial.Blood advances · 2023Trial
- AcTor, a novel mTOR stimulator, potentiates ixazomib for the treatment of acute myeloid leukemia.Molecular cancer · 2026Article
- Prognostic factors influencing outcomes of allogeneic HCT for AML with monosomal karyotype.International journal of hematology · 2026Article
- Article
- Histone methylation defines c-Jun/Sox2/Hif1α axis that controls stemness and tumor progression in squamous cell carcinoma.Nature communications · 2026Article
- AcTor, a novel mTOR stimulator, potentiates ixazomib for the treatment of acute myeloid leukemia.Research square · 2026Article
- The combination therapy with venetoclax in therapeutic strategy of acute lymphoblastic leukemia.Discover oncology · 2026Review
- Mechanisms Underlying Cedazuridine-Mediated Enhancement of Oral Decitabine Bioavailability.Cancer research communications · 2026Article
- Single-molecule tracking of DNMT1 in living cells reveals its cell cycle dynamics and its redistribution upon drug treatment.Nucleic acids research · 2026Article
- Multi-omics based and AI-driven drug repositioning for epigenetic therapy in female malignancies.Journal of translational medicine · 2025Review
- Article
- Efficacy and mechanism of the XPO1 inhibitor selinexor combined with decitabine in T-cell lymphoblastic lymphoma.Annals of hematology · 2025Article
- Epigenetic regulation of angiogenesis and its therapeutics.Genomics & informatics · 2025Review
- PARP inhibitor augments anti-tumor efficacy of DNMT inhibitor by inducing senescence in cholangiocarcinoma.International journal of biological sciences · 2025Article
- PHF6 loss reduces leukemia stem cell activity in an acute myeloid leukemia mouse model.Cancer cell international · 2024Article
- Epigenetic modifications: Key players in cancer heterogeneity and drug resistance.Translational oncology · 2024Article
- DNMT and HDAC inhibition induces immunogenic neoantigens from human endogenous retroviral element-derived transcripts.Nature communications · 2023Article
- Solute Carrier Nucleoside Transporters in Hematopoiesis and Hematological Drug Toxicities: A Perspective.Cancers · 2022Review
- The Role of Histone Post-Translational Modifications in Merkel Cell Carcinoma.Frontiers in oncology · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Decitabine (5-aza-2'-deoxycytidine) is a hypomethylating agent used in the treatment of acute myeloid leukemia (AML). Decitabine inhibits DNA methyltransferases, causing DNA hypomethylation, and leading amongst others to re-expression of silenced tumor suppressor genes. Decitabine is indicated for the treatment of adult patients with newly diagnosed de novo or secondary AML who are not eligible for standard induction chemotherapy. The initial authorization in 2012 was based on the results of the open-label, randomized, multicenter phase 3 DACO-016 trial, and supported by data from the supportive phase 2 open-label DACO-017 trial. Compared with standard care, decitabine significantly improved overall survival, event-free survival, progression-free survival, and response rate. Decitabine was generally well tolerated, offering a valuable treatment option in patients with AML irrespective of age, especially for patients achieving a complete response. Several observational "real-life" studies confirmed these results. In contrast to standard chemotherapy, the presence of adverse-risk karyotypes or TP53 mutations does not negatively impact sensitivity to hypomethylating therapy albeit with lower durability. Data suggest a potential positive effect of decitabine in patients with monosomal karyotype-positive AML. For the time being, decitabine is an appropriate option as monotherapy for patients with AML who are unfit to receive more intensive combination therapies, but emerging data suggest that decitabine-based doublet or triplet combinations may be future treatment options for patients with AML.
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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.