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December 8, 2025Blood

Therapeutic targeting of focal adhesion kinase (FAK) modulates oncogenic and immune pathways in myeloid progenitor cells expressing oncogenic Janus kinase 2-V617F.

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Authors

SNSubbaiah Chary NimmagaddaUniversity Hospital Schleswig-HolsteinMLMorgan LawrenzSchrodinger (United States)EAElena AfanasevaStockholm University

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Implication

Transcriptomic analysis demonstrates focal adhesion kinase modulates apoptosis and immune evasion in myeloproliferative neoplasms, suggesting enhanced treatment strategies with ruxolitinib.

Key Points

  • This research explores the interaction between focal adhesion kinase and JAK2-V617F in myeloproliferative neoplasms.
  • Cultured murine myeloid cells with JAK2 mutation to analyze protein expression.
  • Conducted Western blot for phosphorylation assessment and co-immunoprecipitation for protein interactions.
  • Flow cytometry measured apoptosis and drug synergy evaluated using Coefficient of Drug Interaction.
  • JAK2-V617F activates integrin β1 signaling, implicating focal adhesion kinase in disease mechanisms.
  • FAK phosphorylation was reduced with ruxolitinib treatment, indicating its dependency on JAK2-V617F.
  • Combination of defactinib and ruxolitinib showed enhanced cytotoxic effects and disrupted key survival pathways.

Cite This Study

Nimmagadda et al. (2025) studied this question.

synapsesocial.com/papers/693624d74fa91c937236d0d1https://doi.org/10.1182/blood-2025-3757
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Also Consider

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

  1. 1Disrupting a new NFkB-IL-6-JAK2-STAT cascade with novel NFkB inhibitors reduces primary myelofibrosis growth2025
  2. 2Discovery of JAK2V617F mutant specific allosteric inhibitors for the treatment of myeloproliferative neoplasms2025 · 2 citations
  3. 3Identification of novel, potent, and selective JAK2V617F inhibitors2025 · 1 citations
  4. 4The V617F mutation in JAK2 renders myeloid cells more sensitive to IL-6-mediated gp130 signaling2025
  5. 5Advanced myelofibrosis is marked by loss of NKG2D and DNAM-1 NK activating signaling and increased TIM-3 T CD8 exhaustion2025