ArticleCancer research2017
CTLA4 Promotes Tyk2-STAT3-Dependent B-cell Oncogenicity.
Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 54 citations in OpenAlex.
- Aging and cancer: current understandings and future perspectives.Signal transduction and targeted therapy · 2026Review
- Spatial and phenotypic plasticity of B cells in remodeling the tumor microenvironment.Journal for immunotherapy of cancer · 2026Review
- Immune dysregulation from a novel CTLA-4 haploinsufficiency variant.Journal of human immunity · 2026Article
- Complement contributes to ICI-triggered sialadenitis and predicts ICI efficacy.Cancer immunology, immunotherapy : CII · 2026Article
- Post-translational modifications of immune checkpoints: molecular mechanisms, tumor microenvironment remodeling, and therapeutic implications.Journal of biomedical science · 2026Review
- Correlation betweenJournal of dentistry (Shiraz, Iran) · 2025Article
- Harnessing the power of tumor-draining lymph nodes: unveiling predictive biomarkers for immune checkpoint inhibitor.Exploration of targeted anti-tumor therapy · 2025Review
- Local CpG-Molecular therapy. Nucleic acids · 2024Article
- Immune Checkpoints in B Cells: Unlocking New Potentials in Cancer Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Pan-cancer analysis of STAT3 indicates its potential prognostic value and correlation with immune cell infiltration in prostate cancer.Discover oncology · 2024Article
- Novel STAT3 oligonucleotide compounds suppress tumor growth and overcome the acquired resistance to sorafenib in hepatocellular carcinoma.Acta pharmacologica Sinica · 2024Article
- Exploring the role of histone deacetylase and histone deacetylase inhibitors in the context of multiple myeloma: mechanisms, therapeutic implications, and future perspectives.Experimental hematology & oncology · 2024Review
- Unraveling the complexity of STAT3 in cancer: molecular understanding and drug discovery.Journal of experimental & clinical cancer research : CR · 2024Review
- The positive feedback loop of MAD2L1/TYK2/STAT3 induces progression in B-cell acute lymphoblastic leukaemia.Journal of cancer research and clinical oncology · 2023Article
- PPI Identification of Immune-Related Biomarkers in Esophageal Cancer on the Basis of Gene Co-Expression Network.Iranian journal of biotechnology · 2023Article
- Article
- CTLA-4 and its inhibitors in esophageal cancer: efficacy of therapy and potential mechanisms of adverse events.American journal of cancer research · 2023Review
- The expression and the tumor suppressor role of CLDN6 in colon cancer.Molecular and cellular biochemistry · 2022Article
- Differential regulation of CTLA4 expression through BTK-dependent and independent mechanisms in CLL.Blood advances · 2022Article
- Direct and indirect effects of IFN-α2b in malignancy treatment: not only an archer but also an arrow.Biomarker research · 2022Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
Abstract
CTL-associated antigen 4 (CTLA4) is a well-established immune checkpoint for antitumor immune responses. The protumorigenic function of CTLA4 is believed to be limited to T-cell inhibition by countering the activity of the T-cell costimulating receptor CD28. However, as we demonstrate here, there are two additional roles for CTLA4 in cancer, including via CTLA4 overexpression in diverse B-cell lymphomas and in melanoma-associated B cells. CTLA4-CD86 ligation recruited and activated the JAK family member Tyk2, resulting in STAT3 activation and expression of genes critical for cancer immunosuppression and tumor growth and survival. CTLA4 activation resulted in lymphoma cell proliferation and tumor growth, whereas silencing or antibody-blockade of CTLA4 in B-cell lymphoma tumor cells in the absence of T cells inhibits tumor growth. This inhibition was accompanied by reduction of Tyk2/STAT3 activity, tumor cell proliferation, and induction of tumor cell apoptosis. The CTLA4-Tyk2-STAT3 signal pathway was also active in tumor-associated nonmalignant B cells in mouse models of melanoma and lymphoma. Overall, our results show how CTLA4-induced immune suppression occurs primarily via an intrinsic STAT3 pathway and that CTLA4 is critical for B-cell lymphoma proliferation and survival.
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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.