ReviewInternational journal of hematology2013
Genetic and epigenetic alterations of myeloproliferative disorders.
Review in International journal of hematology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 76 citations in OpenAlex.
- Elevated plasma levels of procoagulant microparticles are a novel risk factor for thrombosis in patients with myeloproliferative neoplasms.International journal of hematology · 2017Trial
- A multinational, open-label, phase 2 study of ruxolitinib in Asian patients with myelofibrosis: Japanese subset analysis.International journal of hematology · 2015Trial
- Non-coding RNAs: Emerging contributors to chemoresistance in chronic myeloid leukemia.Leukemia research reports · 2025Review
- Fusion Genes in Myeloid Malignancies.Cancers · 2024Review
- Molecular Genetics of Thrombotic Myeloproliferative Neoplasms: Implications in Precision Oncology.Diagnostics (Basel, Switzerland) · 2023Review
- Molecular-Targeted Therapy for Tumor-Agnostic Mutations in Acute Myeloid Leukemia.Biomedicines · 2022Review
- The Contribution ofInternational journal of molecular sciences · 2022Review
- Insights into the Potential Mechanisms of JAK2V617F Somatic Mutation Contributing Distinct Phenotypes in Myeloproliferative Neoplasms.International journal of molecular sciences · 2022Review
- TET2, DNMT3A, IDH1, and JAK2 Mutation in Myeloproliferative Neoplasms in southern Iran.International journal of organ transplantation medicine · 2021Article
- Givinostat: an emerging treatment for polycythemia vera.Expert opinion on investigational drugs · 2020Review
- A study to determine the clinical, hematological, cytogenetic, and molecular profile in CML patient in and around Eastern UP, India.Journal of family medicine and primary care · 2019Article
- ASXL1 mutations in Chinese patients with essential thrombocythemia.Experimental and therapeutic medicine · 2018Article
- Health Care Costs and Thromboembolic Events in Hydroxyurea-Treated Patients with Polycythemia Vera.Journal of managed care & specialty pharmacy · 2018Article
- Prevalence of MPL (W515K/L) Mutations in Patients with Negative-JAK2 (V617F) Myeloproliferative Neoplasm in North-East of Iran.Iranian journal of pathology · 2018Article
- Emerging therapeutic targets in myeloproliferative neoplasms and peripheral T-cell leukemia and lymphomas.Expert opinion on therapeutic targets · 2018Review
- Epigenetics in Myeloproliferative Neoplasms.Journal of cellular and molecular medicine · 2017Review
- Article
- Epigenetic changes in myelofibrosis: Distinct methylation changes in the myeloid compartments and in cases with ASXL1 mutations.Scientific reports · 2017Article
- LncRNA SNHG5 regulates imatinib resistance in chronic myeloid leukemia via acting as a CeRNA against MiR-205-5p.American journal of cancer research · 2017Article
- Possible role of intragenic DNA hypermethylation in gene silencing of the tumor suppressor gene NR4A3 in acute myeloid leukemia.Leukemia research · 2016Article
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 2 institutions in 1 country.
Funding
Abstract
The classical BCR-ABL negative myeloproliferative neoplasms (MPN) polycythemia vera, essential thrombocythemia, and primary myelofibrosis are clonal hematopoietic disorders characterized by excessive production of terminally differentiated myeloid cells. In MPN patients, the disease can progress to secondary myelofibrosis or acute myeloid leukemia. Clonal hematopoiesis, disease phenotype, and progression are caused by somatically acquired genetic lesions of genes involved in cytokine signaling, RNA splicing, as well as epigenetic regulation. This review provides an overview of point mutations and cytogenetic lesions associated with MPN and addresses the role of these somatic lesions in MPN disease progression.
Indexed as
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.