ReviewBlood2013
Mutations in epigenetic modifiers in the pathogenesis and therapy of acute myeloid leukemia.
Review in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers, 1 of them a synthesis that pooled it.
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
132 citing papers in PubMed, 1 synthesis or guideline pooled it, 244 citations in OpenAlex.
- Impact of mutations in epigenetic modifiers in acute myeloid leukemia: A systematic review and meta-analysis.Frontiers in oncology · 2022Pooled it
- Trial
- Molecular dissection of valproic acid effects in acute myeloid leukemia identifies predictive networks.Epigenetics · 2016Trial
- Panobinostat as part of induction and maintenance for elderly patients with newly diagnosed acute myeloid leukemia: phase Ib/II panobidara study.Haematologica · 2015Trial
- Epigenetics and In Silico Transcriptome Analysis of Pediatric Acute Myeloid Leukemia.European journal of haematology · 2026Review
- DNA Methylation Dynamics in Development and Disease: Insights from Zebrafish Models.Biomedicines · 2026Review
- Article
- JMJD1C forms condensate to facilitate a RUNX1-dependent gene expression program shared by multiple types of AML cells.Protein & cell · 2025Article
- Identification of HOXA9 methylation as an epigenetic biomarker predicting prognosis and guiding treatment choice in acute myeloid leukemia.BMC cancer · 2025Article
- Prognostic impact of TET2 mutations in patients with acute myeloid leukemia: HM-SCREEN-Japan 01 and 02 study.Annals of hematology · 2025Article
- Engineered sEVs encapsulated in GelMA facilitated diabetic wound healing by promoting angiogenesis via targeting thrombospondin-1.Burns & trauma · 2025Article
- TET2 mutation in acute myeloid leukemia: biology, clinical significance, and therapeutic insights.Clinical epigenetics · 2024Review
- Proteomic profiling reveals ACSS2 facilitating metabolic support in acute myeloid leukemia.Cancer gene therapy · 2024Article
- Identification of Novel DNA Methylation Prognostic Biomarkers for AML With Normal Cytogenetics.JCO clinical cancer informatics · 2024Article
- Chronic myelomonocytic leukemia: 2024 update on diagnosis, risk stratification and management.American journal of hematology · 2024Review
- Clinical Case of Mild Tatton-Brown-Rahman Syndrome Caused by a Nonsense Variant inClinics and practice · 2024Article
- Vemurafenib induces senescence in acute myeloid leukemia and myelodysplastic syndrome by activating the HIPPO signaling pathway: implications for potential targeted therapy.Biology direct · 2024Article
- Genetic Polymorphism Study of IDH 1/2 and TET2 Genes in Acute Myeloid leukemia Patients.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Systematic perturbation of chromatin factors identifies regulatory networks during healthy and malignant hematopoiesis.Nature genetics · 2023Article
- KMT2D Deficiency Promotes Myeloid Leukemias which Is Vulnerable to Ribosome Biogenesis Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
72 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Recent studies of the spectrum of somatic genetic alterations in acute myeloid leukemia (AML) have identified frequent somatic mutations in genes that encode proteins important in the epigenetic regulation of gene transcription. This includes proteins involved in the modification of DNA cytosine residues and enzymes which catalyze posttranslational modifications of histones. Here we describe the clinical, biological, and therapeutic relevance of mutations in epigenetic regulators in AML. In particular, we focus on the role of loss-of-function mutations in TET2, gain-of-function mutations in IDH1 and IDH2, and loss-of-function mutations in ASXL1 and mutations of unclear impact in DNMT3A in AML pathogenesis and therapy. Multiple studies have consistently identified that mutations in these genes have prognostic relevance, particularly in intermediate-risk AML patients, arguing for inclusion of mutational testing of these genetic abnormalities in routine clinical practice. Moreover, biochemical, biological, and epigenomic analyses of the effects of these mutations have informed the development of novel therapies which target pathways deregulated by these mutations. Our understanding of the effects of these mutations on hematopoiesis and potential for therapeutic targeting of specific AML subsets is also reviewed here.
Indexed as
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What OpenQuestion holds
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.