Abstract
Immune-checkpoint inhibitors are firmly established as pillars of cancer therapy, but only a minority of cancer patients currently benefit from these therapies, and therapeutic combinations that can enhance responses are urgently needed. Recently, histone deacetylases (HDACs) have emerged as potential targets for immune modulation, but critical questions remain about their mechanisms of action. In this issue of the JCI, Truong et al. assess whether the HDAC inhibitor entinostat can enhance anti–PD-1 treatment in a bladder cancer model. Entinostat promoted a T cell–inflamed phenotype and had substantial antitumor efficacy when used in combination with anti–PD-1 therapy. In addition, the authors showed that HDAC inhibition augmented tumor neoantigen presentation, resulting in the immune editing of tumor antigens. This study highlights a mechanism by which epigenetic modifier agents can synergize with immune-checkpoint blockade for enhanced and long-lasting antitumor activity.
Original language | English (US) |
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Article number | e151002 |
Journal | Journal of Clinical Investigation |
Volume | 131 |
Issue number | 16 |
DOIs | |
State | Published - Aug 16 2021 |
ASJC Scopus subject areas
- General Medicine