ReviewBlood2023
Biology and therapeutic targeting of molecular mechanisms in MPNs.
Review in Blood, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 64 citations in OpenAlex.
- Obstetric and thrombotic outcomes among pregnant patients with myeloproliferative neoplasms: a propensity score matched real-world analysis.Annals of hematology · 2026Article
- Defining and predicting disease progression in myeloproliferative neoplasms: a proposed biomarker-driven approach.Leukemia · 2026Review
- Article
- Glucose transport dependency defines a therapeutic vulnerability in JAK2V617F-driven myeloproliferative neoplasms.Cell communication and signaling : CCS · 2026Article
- Exploring the mechanism of action of glaucocalyxin D against acute myeloid leukemia using network pharmacology, molecular docking and cellular experiments.Oncology letters · 2026Article
- A paradigm shift in the treatment of patients with polycythemia vera. The initial early use of recombinant interferon-alpha.Leukemia · 2026Review
- A stem and progenitor cell-derived gene expression signature is prognostic for survival in myelofibrosis.Blood · 2026Article
- A Murine Bispecific Antibody Efficiently Redirects T Cells Against Calr Mutated Stem Cells In Vivo.American journal of hematology · 2026Article
- Interleukin-2 and Tretinoin for Myeloproliferative Neoplasms and to Target Type 1 Calreticulin-Driven Neoplasms: Advancements in Immune Regenerative Medicine.International journal of molecular sciences · 2026Article
- Plasma cfDNA and peripheral blood gDNA provide complementary information for molecular monitoring in myeloproliferative neoplasms.Frontiers in oncology · 2026Article
- Gender influences prognosis of classical BCR::ABL1 negative myeloproliferative neoplasms: a retrospective cohort study.Discover oncology · 2025Article
- Review
- Article
- Clinical, morphological and genetic characteristics of patients with concurrent presence of JAK2 V617F and BCR::ABL1.Scientific reports · 2025Article
- Article
- Molecular characterization underlying IFN-α2 treatment in polycythemia vera: a transcriptomic overview.Molecular and cellular biochemistry · 2025Article
- Integrated bioinformatics analysis to develop diagnostic models for malignant transformation of chronic proliferative diseases.Blood science (Baltimore, Md.) · 2025Article
- Dibromo-Edaravone Induces Anti-Erythroleukemia Effects via the JAK2-STAT3 Signaling Pathway.International journal of molecular sciences · 2025Article
- Polycythaemia vera.Nature reviews. Disease primers · 2025Review
- JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Myeloproliferative neoplasms (MPNs) are clonal hematopoietic stem cell disorders characterized by activated Janus kinase (JAK)-signal transducer and activator of transcription signaling. As a result, JAK inhibitors have been the standard therapy for treatment of patients with myelofibrosis (MF). Although currently approved JAK inhibitors successfully ameliorate MPN-related symptoms, they are not known to substantially alter the MF disease course. Similarly, in essential thrombocythemia and polycythemia vera, treatments are primarily aimed at reducing the risk of cardiovascular and thromboembolic complications, with a watchful waiting approach often used in patients who are considered to be at a lower risk for thrombosis. However, better understanding of MPN biology has led to the development of rationally designed therapies, with the goal of not only addressing disease complications but also potentially modifying disease course. We review the most recent data elucidating mechanisms of disease pathogenesis and highlight emerging therapies that target MPN on several biologic levels, including JAK2-mutant MPN stem cells, JAK and non-JAK signaling pathways, mutant calreticulin, and the inflammatory bone marrow microenvironment.
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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.