ArticleCancer science2025
BCL-2 Inhibitor Regulates Number, Function, and Antitumor Immunity of T Cells by Influencing Glycolysis in AML.
Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
- Rosuvastatin enhances the efficacy of venetoclax-azacitidine in older acute myeloid leukemia patients via reducing T-cell exhaustion.Cancer immunology, immunotherapy : CII · 2026Trial
- Venetoclax for elderly patients with acute myeloid leukaemia unfit for intensive chemotherapy: Prospects, resistance mechanisms and management strategies.Clinical and translational medicine · 2026Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
BCL-2 is one of the key genes in the mitochondrial apoptotic pathway, and BCL-2 inhibitor Venetoclax (VEN) is the preferred targeted drug for acute myeloid leukemia (AML) patients. However, the effects of VEN on immune cells and antitumor immune responses in AML patients are poorly understood. We first tested the influence of VEN on AML cells and immune cells. Subsequently, we sorted CD4+ T cells and CD8+ T cells from newly diagnosed AML patients in vitro and constructed a peripheral blood mononuclear cell (PBMC)-humanized AML mouse model to explore the effects of VEN on the T cell number, function, and antitumor immune responses, while actively seeking potential mechanisms. VEN could effectively induce leukemia cell apoptosis and affect the lymphocyte proportion and cytokine levels in the tumor immune microenvironment of AML. T cells of AML patients had apoptosis resistance to VEN, possibly due to their relatively low expression levels of BCL-2 protein. VEN could regulate the secretory function and activation status of T cells in AML, which mainly manifested in promoting IFN-γ and Perforin and Granzyme B secretion, upregulating PD-1 expression, promoting T cell activation, and increasing the proportion of memory T cells. Finally, it was also observed that VEN could enhance T cell-mediated antitumor immune responses in AML. Mechanistically, VEN modulates the glycolysis pathway of T cells to regulate their number, function, and antitumor immune responses. This research provided a new perspective that molecular-targeted drugs can promote tumor cell death through a unique immune-dependent mechanism.
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Registered trials
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.