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December 8, 2025Blood

Transcriptomic analysis of CD34⁺ cells in myelofibrosis highlights their role in extracellular matrix dysregulation and marrow fibrosis

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Authors

LGLuca GaruffoCCCecilia Carubbi

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Overview

RNASeq analysis reveals cell adhesion and wound healing pathways in CD34+ cells from myelofibrosis, highlighting their role in extracellular matrix dysregulation.

Key Points

  • The study aims to elucidate the role of CD34+ cells in myelofibrosis through transcriptomic analysis, focusing on extracellular matrix dysregulation.
  • Performed RNASeq analysis on immunomagnetically isolated CD34+ cells from myelofibrosis patients and healthy donors.
  • Compared gene expression across different myelofibrosis subtypes and fibrosis grades, along with JAK-inhibitor therapy effects.
  • Conducted pathway enrichment analysis using GeneOntology and KEGG.
  • Identified 8353 differentially expressed genes among naïve myelofibrosis patients and healthy controls.
  • Highlighted enriched pathways linked to wound healing, extracellular matrix remodeling, and cell adhesion.
  • Demonstrated significant alterations in integrin and collagen gene expressions depending on fibrosis severity and JAK-inhibitor therapy.

Cite This Study

Garuffo et al. (2025) studied this question.

synapsesocial.com/papers/69362f7f4fa91c937236e593https://doi.org/10.1182/blood-2025-5535
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Also Consider

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

  1. 1Quantitative profiling and clinical correlative analysis of fibrocytes and mesenchymal stromal cells in myelofibrosis spleen2025
  2. 2Integrated transcriptome-proteome analysis in patients with myelofibrosis-related anemia2026
  3. 3Advanced myelofibrosis is marked by loss of NKG2D and DNAM-1 NK activating signaling and increased TIM-3 T CD8 exhaustion2025
  4. 4Fibrocytes drive JAK2V617F-mutated myelofibrosis: pitavastatin reverses marrow fibrosis and anemia2026
  5. 5Identification of biomarkers to predict disease progression via molecular analysis of patients (pts) with low-risk myelofibrosis (MF) enrolled in the MOST study2025