ReviewInternational journal of molecular sciences2024
Senescent T Cells: The Silent Culprit in Acute Myeloid Leukemia Progression?
Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
2 citing papers in PubMed.
- SIX1 drives acute myeloid leukemia progression by reprogramming glycolytic metabolism and impairing CD8⁺ T-cell effector function.Immunologic research · 2026Article
- Lactylation modification regulates acute myeloid leukemia pathogenesis and immune microenvironment.Discover oncology · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Malignant tumors can evade immune surveillance and elimination through multiple mechanisms, with the induction of immune cell dysfunction serving as a crucial strategy. Mounting evidence indicates that T cell senescence constitutes the primary mechanism underlying T cell dysfunction in acute myeloid leukemia (AML) and represents one of the potential causes of immunotherapy failure. AML usually progresses rapidly and is highly susceptible to drug resistance, thereby resulting in recurrence and patient mortality. Hence, disrupting the immune interface within the bone marrow microenvironment of AML has emerged as a critical objective for synergistically enhancing tumor immunotherapy. In this review, we summarize the general characteristics, distinctive phenotypes, and regulatory signaling networks of senescent T cells and highlight their potential clinical significance in the bone marrow microenvironment of AML. Additionally, we discuss potential therapeutic strategies for alleviating and reversing T cell senescence.
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Registered trials
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