01624nam a2200241 4500 ESSALUD 20260805102227.0 ta t pe ||||| |||| 00| 0 spa d BMG eng Hotchkiss, Richard S. Autor 53924 Stemness as the engine of checkpoint durability páginas: 2374-2377 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. CANCER 1231 GENÉTICA 1105 HEMATOLOGÍA 7422 INMUNIDAD 38590 DiPersio, John F. 53925 22717 22640 Massachusetts NEJM Group NEJM007 The New England Journal of Medicine ESSALUD 0028-4793 ARTICULOS 2026-08-03 SQB 22772 22772