Hotchkiss, Richard S. creator Autor DiPersio, John F. text pe monographic spa eng

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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 GENÉTICA HEMATOLOGÍA INMUNIDAD Massachusetts NEJM Group NEJM007 0028-4793 ESSALUD BMG 20260805102227.0 ESSALUD