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040			_aBMG
041			_aeng
100			_aHotchkiss, Richard S. _eAutor _953924
245			_aStemness as the engine of checkpoint durability
300			_apáginas: 2374-2377
520			_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.
650			_aCANCER _91231
650			_aGENÉTICA _91105
650			_aHEMATOLOGÍA _97422
650			_aINMUNIDAD _938590
700			_aDiPersio, John F. _953925
773	0		_022717 _922640 _dMassachusetts NEJM Group _oNEJM007 _tThe New England Journal of Medicine _wESSALUD _x0028-4793
942			_cARTICULOS _e2026-08-03 _zSQB
999			_c22772 _d22772