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One state is enriched for markers of activation, whereas the other expresses natural killer (NK)-like and senescence markers. The skewed clonal differentiation trajectory toward CD8+ senescence was also a hallmark indicative of therapy resistance. We validated these findings by generating an AML CD8+ single-cell atlas integrating our data and other independent data sets. Finally, our analysis revealed that an imbalance between CD8+ early memory and senescent-like cells is linked to AML treatment refractoriness and poor survival. Our study provides crucial insights into the dynamics of CD8+ T-cell differentiation and advances our understanding of CD8+ T-cell dysfunction in AML.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2023021680","type":"journal-article","created":{"date-parts":[[2024,5,22]],"date-time":"2024-05-22T15:56:51Z","timestamp":1716393411000},"page":"1168-1182","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":46,"title":["CD8+ T-cell differentiation and dysfunction inform treatment response in acute myeloid leukemia"],"prefix":"10.1182","volume":"144","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6126-8719","authenticated-orcid":false,"given":"Francesco","family":"Mazziotta","sequence":"first","affiliation":[{"name":"1Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD"},{"name":"2Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, 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