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December 8, 2025BloodOpen Access

Unravelling molecular determinants of ruxolitinib treatment response in myelofibrosis using single cell multiomics

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Authors

SPSandra ParentiDBDaniela BenatiANAnita Neroni

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Overview

Analysis reveals treatment response in myelofibrosis linked to epigenetic regulators and cellular dynamics.

Key Points

  • To identify molecular determinants related to response to ruxolitinib in myelofibrosis patients.
  • Used single-cell genomics and proteomics to analyze 12 MF patients during ruxolitinib treatment.
  • Patients classified as responders or non-responders based on clinical symptoms and treatment outcome.
  • Blood samples collected, and cells stained to analyze genetic mutations.
  • Conducted differential gene expression analysis to study signaling pathways.
  • Ruxolitinib treatment reduced CD34+ hematopoietic stem and progenitor cells in responders but increased in non-responders.
  • Differential gene expression indicated increased JAK/STAT signaling in non-responder monocytes.
  • Most frequently mutated genes included epigenetic regulators like TET2 and ASXL1.

Cite This Study

Parenti et al. (2025) studied this question.

synapsesocial.com/papers/693624d74fa91c937236d126https://doi.org/10.1182/blood-2025-3750
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Genome-wide CRISPR-Cas9 screen reveals novel ruxolitinib-resistance targets in myeloproliferative neoplasms2025
  2. 2Dose intensive regimen of CK0804 tregs in myelofibrosis2025
  3. 3Clonal architecture inferred from routine NGS data predicts outcome and response to JAK-inhibitors in myelofibrosis2025
  4. 4A phase I study of the combination of ruxolitinib and the ERK1/2 inhibitor ulixertinib in previously treated myelofibrosis patients.2025
  5. 5Single-cell transcriptomic studies reveal altered heterogeneity in CD41 enriched megakaryocytes after targeted therapy in myeloproliferative neoplasm2025