ArticleBlood2024
CD8+ T-cell differentiation and dysfunction inform treatment response in acute myeloid leukemia.
Article in Blood, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed.
- A phase I/II trial of WT1-specific TCR gene therapy for patients with acute myeloid leukemia and active disease post-allogeneic hematopoietic cell transplantation: skewing towards NK-like phenotype impairs T cell function and persistence.Nature communications · 2025Trial
- SIX1 drives acute myeloid leukemia progression by reprogramming glycolytic metabolism and impairing CD8⁺ T-cell effector function.Immunologic research · 2026Article
- Sequential in vivo CRISPR screens identify the clonal dominance ofBlood science (Baltimore, Md.) · 2026Article
- T cell-engaging bispecific antibodies for myeloid malignancies: Targets, formats, and clinical challenges.Cell reports. Medicine · 2026Review
- A Three-Gene Interferon Signature Predicts Sustained Complete Remission in Pediatric AML Patients.Cancers · 2026Article
- Integrated multi-target pharmacology of ginseng in acute myeloid leukemia through single-cell sequencing, molecular docking, network pharmacology, and in vitro experiments.Discover oncology · 2026Article
- Venetoclax combined with ML385 overcomes chemotherapy resistance in acute myeloid leukemia by modulating Nrf2/ARE-mediated oxidative stress.Medical oncology (Northwood, London, England) · 2026Article
- From monoclonals to bispecific T cell engagers: the evolving antibody-based therapy landscape in acute myeloid leukemia.Frontiers in immunology · 2026Review
- Beyond exhaustion: T cell fitness for next generation of immunotherapy for hematological cancer.Frontiers in immunology · 2026Review
- Associations of polymorphisms in the myeloid immunoregulatory receptor gene MRC1 with expression and prognosis in acute myeloid leukemia.Frontiers in immunology · 2026Article
- Crosstalk of cancer stemness-neutrophils in outcome of intracranial germ cell tumors.Frontiers in immunology · 2026Article
- Review
- Lactylation modification regulates acute myeloid leukemia pathogenesis and immune microenvironment.Discover oncology · 2025Article
- Aberrant expression of SLAMF6 constitutes a targetable immune escape mechanism in acute myeloid leukemia.Nature cancer · 2025Article
- Bone marrow lymphocyte dynamics during chemotherapy in pediatric acute myeloid leukemia.HemaSphere · 2025Article
- Comprehensive profiling of AML and T-cell states across disease stages in acute myeloid leukemia using spectral flow cytometry.Blood immunology & cellular therapy · 2025Article
- Therapeutic hurdles in acute myeloid leukemia: Leukemic stem cells, inflammation and immune dysfunction.Current opinion in pharmacology · 2025Review
- SOCS1 Protects Acute Myeloid Leukemia against Allogeneic T Cell-Mediated Cytotoxicity.Blood cancer discovery · 2025Article
- The Emerging Role of CD8Cancers · 2025Review
- Single-cell profiling uncovers PTPRG-driven stemness in malignant plasma cells and signatures of treatment failure in multiple myeloma.Frontiers in immunology · 2025Article
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16 authors.
Funding
Abstract
abstractThe interplay between T-cell states of differentiation, dysfunction, and treatment response in acute myeloid leukemia (AML) remains unclear. Here, we leveraged a multimodal approach encompassing high-dimensional flow cytometry and single-cell transcriptomics and found that early memory CD8+ T cells are associated with therapy response and exhibit a bifurcation into 2 distinct terminal end states. 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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.