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Related Experiment Video

Updated: Jul 31, 2025

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Metabolic Reprogramming by Histone Deacetylase Inhibition Selectively Targets NRF2-activated tumors.

Dimitris Karagiannis, Warren Wu, Albert Li

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    Lung adenocarcinoma with NRF2 activation becomes vulnerable to histone deacetylase (HDAC) inhibition. This cancer vulnerability is linked to metabolic pathway alterations, suggesting HDAC inhibitors could treat NRF2-active solid tumors.

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    Area of Science:

    • Oncology
    • Epigenetics
    • Metabolism

    Background:

    • Metabolism and chromatin signaling interplay in cancer progression.
    • Aberrant NRF2 pathway activation in lung adenocarcinoma (LUAD) drives aggressive, chemo-resistant disease.
    • Epigenetic vulnerabilities arising from tumor metabolic reprogramming remain unclear.

    Conclusions:

    • Metabolic alterations, like NRF2 activation, create epigenetic vulnerabilities to HDAC inhibitors in LUAD.
    • NRF2 activation may serve as a biomarker for repurposing HDAC inhibitors in solid tumors.
    • Targeting HDACs offers a potential therapeutic strategy for NRF2-driven cancers.