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December 8, 2025Blood

Shared mechanisms of resistance to zanubrutinib and ibrutinib via EGR1 and DNMT3A in mantle cell lymphoma

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Authors

LRLixin RuiUniversity of Wisconsin–Madison

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Implication

Analysis reveals DNMT3A and mitochondrial metabolism drive resistance to ibrutinib in mantle cell lymphoma, suggesting metformin may enhance treatment efficacy.

Key Points

  • This research aims to investigate the shared resistance mechanisms to BTK inhibitors in mantle cell lymphoma.
  • Identified EGR1 and DNMT3A as mediators of ibrutinib resistance.
  • Analyzed their role in mitochondrial metabolism and drug sensitivity dynamics.
  • Examined the effects of IM156, a metformin analog, on drug efficacy in vitro.
  • EGR1 and DNMT3A expression levels were elevated in ibrutinib-resistant MCL cells.
  • Targeting these genes restored drug sensitivity in resistant cells.
  • IM156 combined with zanubrutinib showed synergistic effects in inducing cell death.

Cite This Study

Lixin Rui (2025) studied this question.

synapsesocial.com/papers/69362f484fa91c937236d696https://doi.org/10.1182/blood-2025-7075
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Also Consider

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

  1. 1Targeting DNMT3A-mediated oxidative phosphorylation to overcome ibrutinib resistance in mantle cell lymphoma2024 · 16 citations
  2. 2EGR1-mediated metabolic reprogramming to oxidative phosphorylation contributes to ibrutinib resistance in B-cell lymphoma2023 · 50 citations
  3. 3Loss of miR-146a-5p contributes to ibrutinib resistance in mantle cell lymphoma2026
  4. 4Cyclin-dependent kinase-9 and oxidative phosphorylation inhibition overcome ibrutinib resistance in mantle cell lymphoma.2026
  5. 5Strategies for overcoming resistance to Bruton's tyrosine kinase inhibitor zanubrutinib2024 · 6 citations