Observational studyBlood2021
Inferring the dynamics of mutated hematopoietic stem and progenitor cells induced by IFNα in myeloproliferative neoplasms.
Observational study in Blood, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05850273 (Mechanism of Action of Interferon in the Treatment of Myeloproliferative Neoplasms), which is not on this map. Cited by 32 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.
Mechanism of Action of Interferon in the Treatment of Myeloproliferative Neoplasms
Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- Type 1 interferon perturbates clonal competition by reshaping human blood development.Nature genetics · 2026Article
- Mathematical modeling ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- [Comparative study of the prognostic value of survival prognostic scoring systems in patients with essential thrombocythemia: IPSET, MIPSS-ET, AAA, and AAA].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Article
- Interferon in early MF: intersection of biology and evidence.Blood advances · 2026Article
- A paradigm shift in the treatment of patients with polycythemia vera. The initial early use of recombinant interferon-alpha.Leukemia · 2026Review
- Novel strategies targeting mutant calreticulin in essential thrombocythemia and myelofibrosis.Blood · 2026Review
- Modeling the evolutionary dynamics of clonal hematopoiesis.Nature genetics · 2026Review
- Sabotaged Integral HSC Heterogeneity Underlies Essential Thrombocythemia Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Plasma cfDNA and peripheral blood gDNA provide complementary information for molecular monitoring in myeloproliferative neoplasms.Frontiers in oncology · 2026Article
- Rapid Hematological and Molecular Response to Pegylated Interferon in WHO-Defined Pre-Fibrotic Myelofibrosis.Cancers · 2025Article
- The Dual Role of Interferon Signaling in Myeloproliferative Neoplasms: Pathogenesis and Targeted Therapeutics.Cancers · 2025Review
- Deciphering the complex clonal heterogeneity of polycythemia vera and the response to interferon alfa.Blood advances · 2025Article
- New approaches to standard of care in early-phase myeloproliferative neoplasms: can interferon-α alter the natural history of the disease?Haematologica · 2025Review
- Mutant Calreticulin in MPN: Mechanistic Insights and Therapeutic Implications.Current hematologic malignancy reports · 2025Review
- Pegylated interferon: the who, why, and how.Hematology. American Society of Hematology. Education Program · 2024Review
- Investigational drugs in early phase trials for myelofibrosis.Expert opinion on investigational drugs · 2024Review
- Myeloproliferative neoplasms: young patients, current data and future considerations.Annals of hematology · 2024Article
- Molecular Genetic Profile of Myelofibrosis: Implications in the Diagnosis, Prognosis, and Treatment Advancements.Cancers · 2024Review
- Mathematical modelling of stem and progenitor cell dynamics during ruxolitinib treatment of patients with myeloproliferative neoplasms.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
28 authors at 9 institutions in 5 countries.
Funding
Abstract
Classical BCR-ABL-negative myeloproliferative neoplasms (MPNs) are clonal disorders of hematopoietic stem cells (HSCs) caused mainly by recurrent mutations in genes encoding JAK2 (JAK2), calreticulin (CALR), or the thrombopoietin receptor (MPL). Interferon α (IFNα) has demonstrated some efficacy in inducing molecular remission in MPNs. To determine factors that influence molecular response rate, we evaluated the long-term molecular efficacy of IFNα in patients with MPN by monitoring the fate of cells carrying driver mutations in a prospective observational and longitudinal study of 48 patients over more than 5 years. We measured the clonal architecture of early and late hematopoietic progenitors (84 845 measurements) and the global variant allele frequency in mature cells (409 measurements) several times per year. Using mathematical modeling and hierarchical Bayesian inference, we further inferred the dynamics of IFNα-targeted mutated HSCs. Our data support the hypothesis that IFNα targets JAK2V617F HSCs by inducing their exit from quiescence and differentiation into progenitors. Our observations indicate that treatment efficacy is higher in homozygous than heterozygous JAK2V617F HSCs and increases with high IFNα dose in heterozygous JAK2V617F HSCs. We also found that the molecular responses of CALRm HSCs to IFNα were heterogeneous, varying between type 1 and type 2 CALRm, and a high dose of IFNα correlates with worse outcomes. Our work indicates that the long-term molecular efficacy of IFNα implies an HSC exhaustion mechanism and depends on both the driver mutation type and IFNα dose.
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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.