01627nam a2200241   4500001000800000005001700008007000300025008004100028040000800069041000800077100004100085245005200126300002500178520091100203650001701114650002101131650002401152650002101176700003001197773011001227942003101337999001701368ESSALUD20260805102227.0ta      t        pe ||||| |||| 00| 0 spa d  aBMG  aeng  aHotchkiss, Richard S. eAutor953924  aStemness as the engine of checkpoint durability  apáginas: 2374-2377  aCheckpoint 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.  aCANCER91231  aGENÉTICA91105  aHEMATOLOGÍA97422  aINMUNIDAD938590  aDiPersio, John F. 9539250 022717922640dMassachusetts NEJM GroupoNEJM007tThe New England Journal of Medicine wESSALUDx0028-4793  cARTICULOSe2026-08-03zSQB  c22772d22772