ArticleProceedings of the National Academy of Sciences of the United States of America2009
E(mu)-TCL1 mice represent a model for immunotherapeutic reversal of chronic lymphocytic leukemia-induced T-cell dysfunction.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
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Who cites it
82 citing papers in PubMed, 125 citations in OpenAlex.
- Lenalidomide in nonmetastatic biochemically relapsed prostate cancer: results of a phase I/II double-blinded, randomized study.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010Trial
- Mitigating T-cell mitochondrial dysfunction in CLL to augment CAR T-cell therapy: evaluation in an immunocompetent model.Blood advances · 2025Article
- Article
- The Elevation and Impact of Peripheral Bile Acids in Chronic Lymphocytic Leukemia.Biomedicines · 2025Article
- Impact of mitochondrial metabolism on T-cell dysfunction in chronic lymphocytic leukemia.Frontiers in cell and developmental biology · 2025Review
- Immunogenic Cell Death Traits Emitted from Chronic Lymphocytic Leukemia Cells Following Treatment with a Novel Anti-Cancer Agent, SpiD3.Biomedicines · 2024Article
- Increased Frequency of Circulating Activated FOXP3Cancers · 2024Article
- Targeting chronic lymphocytic leukemia with B-cell activating factor receptor CAR T cells.MedComm · 2024Article
- BET inhibition reforms the immune microenvironment and alleviates T cell dysfunction in chronic lymphocytic leukemia.JCI insight · 2024Article
- The Role of the Microenvironment and Cell Adhesion Molecules in Chronic Lymphocytic Leukemia.Cancers · 2023Review
- The role of Th17 cells in chronic lymphocytic leukemia: friend or foe?Blood advances · 2023Review
- Proinflammatory microenvironment promotes lymphoma progression in mice with high megakaryocyte and TPO levels.Blood advances · 2023Article
- T cell receptor gene repertoire profiles in subgroups of patients with chronic lymphocytic leukemia bearing distinct genomic aberrations.Frontiers in oncology · 2023Article
- Differential regulation of CTLA4 expression through BTK-dependent and independent mechanisms in CLL.Blood advances · 2022Article
- Enhanced Costimulatory Signaling Improves CAR T-cell Effector Responses in CLL.Cancer research communications · 2022Article
- Article
- In Vitro and In Vivo Models of CLL-T Cell Interactions: Implications for Drug Testing.Cancers · 2022Review
- Regulatory T cells (Tregs) in lymphoid malignancies and the impact of novel therapies.Frontiers in immunology · 2022Review
- Combined ibrutinib and venetoclax treatment vs single agents in the TCL1 mouse model of chronic lymphocytic leukemia.Blood advances · 2021Article
- CD4+ T cells sustain aggressive chronic lymphocytic leukemia in Eμ-TCL1 mice through a CD40L-independent mechanism.Blood advances · 2021Article
22 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Preclinical animal models have largely ignored the immune-suppressive mechanisms that are important in human cancers. The identification and use of such models should allow better predictions of successful human responses to immunotherapy. As a model for changes induced in nonmalignant cells by cancer, we examined T-cell function in the chronic lymphocytic leukemia (CLL) Emu-TCL1 transgenic mouse model. With development of leukemia, Emu-TCL1 transgenic mice developed functional T-cell defects and alteration of gene and protein expression closely resembling changes seen in CLL human patients. Furthermore, infusion of CLL cells into young Emu-TCL1 mice induced defects comparable to those seen in mice with developed leukemia, demonstrating a causal relationship between leukemia and the T-cell defects. Altered pathways involved genes regulating actin remodeling, and T cells exhibited dysfunctional immunological synapse formation and T-cell signaling, which was reversed by the immunomodulatory drug lenalidomide. These results further demonstrate the utility of this animal model of CLL and define a versatile model to investigate both the molecular mechanisms of cancer-induced immune suppression and immunotherapeutic repair strategies.
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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.