ArticleNature communications2025
Efficacy of JAK1/2 inhibition in murine myeloproliferative neoplasms is not mediated by targeting oncogenic signaling.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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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.
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Who cites it
7 citing papers in PubMed.
- Review
- Menin-dependent megakaryocyte proliferation and fibrosis in myeloproliferative neoplasms.Cancer cell · 2026Article
- The bidirectional relationship betweenHemaSphere · 2026Article
- Novel and emerging therapeutic strategies for clonal hematopoiesis.Haematologica · 2026Review
- [Myeloproliferative neoplasm with a homozygous germline SH2B3 mutation: a case report and literature review].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Review
- Neutrophil-to-lymphocyte ratio as a gene-specific biomarker of JAK2-driven inflammation across CHIP and myeloproliferative neoplasms.Frontiers in oncology · 2026Article
- Oncostatin M induced by STAT5-activating oncogenes promotes disease progression in hematologic malignancies.Signal transduction and targeted therapy · 2025Article
Corrections and comments
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Authors and funding
23 authors.
Funding
Abstract
Ruxolitinib is a potent JAK1/JAK2 inhibitor, approved for the treatment of primary myelofibrosis (PMF) patients based on the concept of inhibition of oncogenic signaling. However, the effect of ruxolitinib on JAK2-V617F allelic burden is modest, suggesting that inhibition of JAK2-V617F signaling-driven clone expansion is not the main mechanism of action. We evaluate whether ruxolitinib mainly blocks the proliferation of the malignant clone or exerts its effects also by targeting non-malignant cells. Therefore, we develop two JAK2-V617F-driven myeloproliferative neoplasm (MPN) mouse models harboring ruxolitinib resistance mutations. Mice carrying ruxolitinib-resistant JAK2-V617F-driven MPN respond to ruxolitinib treatment similar to mice with ruxolitinib-sensitive JAK2-V617F MPN with respect to reduction of spleen size, leukocyte count and pro-inflammatory cytokines in the serum. Ruxolitinib reduces pro-inflammatory cytokines in both stromal cells and non-malignant hematopoietic cells. Using a rigorous ruxolitinib resistance mutation approach, we can prove that ruxolitinib acts independent of oncogenic JAK2-V617F signaling and reduces the main features of MPN disease such as spleen size and leukocyte counts. Our findings characterize the mechanism of action for ruxolitinib in MPN.
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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.