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December 8, 2025BloodOpen Access

Clonal architecture inferred from routine NGS data predicts outcome and response to JAK-inhibitors in myelofibrosis

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Authors

AEAlessio EndertiGLGiuseppe Gaetano LoscoccoMBMassimo Breccia

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Overview

Investigation finds clonal evolution impacts splenomegaly response in myelofibrosis patients treated with JAK inhibitors.

Key Points

  • This research aims to explore how clonal architecture correlates with treatment outcomes in myelofibrosis patients using JAK inhibitors.
  • Analyzed data from all JAKi-treated myelofibrosis patients in the database.
  • Conducted mutation analysis of 40 myeloid neoplasm-associated genes via next-generation sequencing.
  • Classified mutations into functional categories and assessed clonal architecture using variant allele frequency.
  • Calculated the Shannon Diversity Index for clonal diversity assessment, categorizing patients based on median values.
  • Out of 250 JAKi-treated patients, 47.8% achieved spleen response.
  • Age below 65 years and absence of certain mutations were associated with better spleen response.
  • Clonal evolution was linked to treatment responses and overall survival, highlighting its prognostic importance.

Cite This Study

Enderti et al. (2025) studied this question.

synapsesocial.com/papers/693624d74fa91c937236d118https://doi.org/10.1182/blood-2025-3753
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Also Consider

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

  1. 1Mutational architecture and clonal heterogeneity in myelofibrosis: Prognostic role of variant type and acquisition sequence2025
  2. 2Unravelling molecular determinants of ruxolitinib treatment response in myelofibrosis using single cell multiomics2025 · 1 citations
  3. 3Long-term outcome and risk factors for relapse after allogeneic hematopoietic stem cell transplantation in myelofibrosis: Results from a large multicenter cohort2025
  4. 4Quantitative profiling and clinical correlative analysis of fibrocytes and mesenchymal stromal cells in myelofibrosis spleen2025
  5. 5Advanced myelofibrosis is marked by loss of NKG2D and DNAM-1 NK activating signaling and increased TIM-3 T CD8 exhaustion2025