ArticleClinical epigenetics2011
Epigenetic abnormalities in myeloproliferative neoplasms: a target for novel therapeutic strategies.
Article in Clinical epigenetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 48 citations in OpenAlex.
- A potent dual inhibitor targeting COX-2 and HDAC of acute myeloid leukemia cells.Molecular diversity · 2025Article
- Current Advances in the Diagnosis and Treatment of Major Myeloproliferative Neoplasms.Cancers · 2025Review
- DNA Methylation in Ph-Negative Myeloproliferative Neoplasms: Prognostic Role and Therapeutic Implications.Current issues in molecular biology · 2025Review
- Molecular Genetics of Thrombotic Myeloproliferative Neoplasms: Implications in Precision Oncology.Diagnostics (Basel, Switzerland) · 2023Review
- Understanding Aberrant Signaling to Elude Therapy Escape Mechanisms in Myeloproliferative Neoplasms.Cancers · 2022Review
- Platelet transcriptome identifies progressive markers and potential therapeutic targets in chronic myeloproliferative neoplasms.Cell reports. Medicine · 2021Article
- Epigenetic Control of Infant B Cell Precursor Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2021Review
- Novel therapeutics in myeloproliferative neoplasms.Journal of hematology & oncology · 2020Review
- Cotargeting the JAK/STAT signaling pathway and histone deacetylase by ruxolitinib and vorinostat elicits synergistic effects against myeloproliferative neoplasms.Investigational new drugs · 2020Article
- Givinostat: an emerging treatment for polycythemia vera.Expert opinion on investigational drugs · 2020Review
- MIR-144-mediated NRF2 gene silencing inhibits fetal hemoglobin expression in sickle cell disease.Experimental hematology · 2019Article
- The Role of New Technologies in Myeloproliferative Neoplasms.Frontiers in oncology · 2019Review
- Article
- HSP27 is a partner of JAK2-STAT5 and a potential therapeutic target in myelofibrosis.Nature communications · 2018Article
- The role of the extracellular matrix in primary myelofibrosis.Blood cancer journal · 2017Review
- Investigational histone deacetylase inhibitors (HDACi) in myeloproliferative neoplasms.Expert opinion on investigational drugs · 2016Review
- A data-driven network model of primary myelofibrosis: transcriptional and post-transcriptional alterations in CD34+ cells.Blood cancer journal · 2016Article
- Evolving Therapeutic Strategies for the Classic Philadelphia-Negative Myeloproliferative Neoplasms.EBioMedicine · 2016Review
- Clinical potential of pacritinib in the treatment of myelofibrosis.Therapeutic advances in hematology · 2015Review
- Novel therapies for myelofibrosis.Leukemia & lymphoma · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The myeloproliferative neoplasms (MPNs) are a group of clonal hematological malignancies characterized by a hypercellular bone marrow and a tendency to develop thrombotic complications and to evolve to myelofibrosis and acute leukemia. Unlike chronic myelogenous leukemia, where a single disease-initiating genetic event has been identified, a more complicated series of genetic mutations appear to be responsible for the BCR-ABL1-negative MPNs which include polycythemia vera, essential thrombocythemia, and primary myelofibrosis. Recent studies have revealed a number of epigenetic alterations that also likely contribute to disease pathogenesis and determine clinical outcome. Increasing evidence indicates that alterations in DNA methylation, histone modification, and microRNA expression patterns can collectively influence gene expression and potentially contribute to MPN pathogenesis. Examples include mutations in genes encoding proteins that modify chromatin structure (EZH2, ASXL1, IDH1/2, JAK2V617F, and IKZF1) as well as epigenetic modification of genes critical for cell proliferation and survival (suppressors of cytokine signaling, polycythemia rubra vera-1, CXC chemokine receptor 4, and histone deacetylase (HDAC)). These epigenetic lesions serve as novel targets for experimental therapeutic interventions. Clinical trials are currently underway evaluating HDAC inhibitors and DNA methyltransferase inhibitors for the treatment of patients with MPNs.
Identifiers
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.