Stemness as the engine of checkpoint durability
Por: Hotchkiss, Richard S [Autor]
Colaborador(es): DiPersio, John FTipo de material: 
TextoIdioma: Inglés Descripción: páginas: 2374-2377Tema(s): CANCER | GENÉTICA | HEMATOLOGÍA | INMUNIDAD
En: The New England Journal of MedicineResumen: Checkpoint inhibitors have transformed cancer therapy, with 250,000 to 400,000 patients treated annually in the United States. By blocking programmed cell death protein 1 (PD-1) or its ligand (PD-L1), checkpoint inhibitors suppress inhibitory signals that restrain T-cell activation, thereby restoring antitumor immunity. Despite early and sometimes dramatic responses, clinical benefits often wane. Retrospective analyses of checkpoint-inhibitor rechallenge show lower response rates and diminished durability as compared with initial treatment. These observations lead to the question: can prolonged or intensified PD-1 or PD-L1 blockade paradoxically compromise the long-term immune fitness required for sustained tumor control? A recent study by Hor et al. suggests that it does and provides a mechanistic framework that may reshape how checkpoint inhibitors are deployed and their durability extended.
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Títulos de Revistas
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Biblioteca Central ESSALUD | Colección General | NEJM (Navegar estantería) | Vol.394, No.23 (2026) | Disponible | NEJM007 |
Checkpoint inhibitors have transformed cancer therapy, with 250,000 to 400,000 patients treated annually in the United States. By blocking programmed cell death protein 1 (PD-1) or its ligand (PD-L1), checkpoint inhibitors suppress inhibitory signals that restrain T-cell activation, thereby restoring antitumor immunity. Despite early and sometimes dramatic responses, clinical benefits often wane. Retrospective analyses of checkpoint-inhibitor rechallenge show lower response rates and diminished durability as compared with initial treatment. These observations lead to the question: can prolonged or intensified PD-1 or PD-L1 blockade paradoxically compromise the long-term immune fitness required for sustained tumor control? A recent study by Hor et al. suggests that it does and provides a mechanistic framework that may reshape how checkpoint inhibitors are deployed and their durability extended.