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December 8, 2025BloodOpen Access

NSD2 inhibition suppresses t(4;14) gene expression and oncogenic signaling to impair proliferation in multiple myeloma

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Authors

RCRobert S. ChavezTCTerry Connolly

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Overview

Inhibition of NSD2 reduced chromatin marks and oncogenic signaling in multiple myeloma, suggesting a new therapeutic target.

Key Points

  • NSD2 inhibition depleted H3K36me2, impacting gene expression and growth of myeloma cells.
  • Gene Set Enrichment Analysis revealed NSD2's role in regulating proto-oncogenes and chromatin dynamics.
  • CRISPR/Cas9 disruption of NSD2 enhanced understanding of its oncogenic function in multiple myeloma.
  • Findings point to potential clinical applications in targeting NSD2 for treating multiple myeloma.

Cite This Study

Chavez et al. (2025) studied this question.

synapsesocial.com/papers/69362f364fa91c937236d36dhttps://doi.org/10.1182/blood-2025-3956
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Also Consider

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

  1. 1NSD2 expression remodels DNA methylation, creating a targetable epigenetic dependency in t(4;14) multiple myeloma2025
  2. 2Inhibition of NSD2 in t(4;14) myeloma induces changes in mitochondrial priming2025
  3. 3Comprehensive pan-cancer analysis identified NSD2 as a potential prognostic and diagnostic biomarker2025
  4. 4Cyclin D1 beyond the cell cycle: A new role in t(11;14) multiple myeloma2025
  5. 5Ktx-1001, a potent, selective MMSET/NSD2 inhibitor, enhances immunomodulatory and immune-directed therapies in preclinical models of multiple myeloma2025