ArticleFrontiers in immunology2023
Antigen presentation deficiency, mesenchymal differentiation, and resistance to immunotherapy in the murine syngeneic CT2A tumor model.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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Who cites it
24 citing papers in PubMed, 20 citations in OpenAlex.
- Tumor infiltrating lymphocytes in glioblastoma: immunobiology and translational implications.NPJ precision oncology · 2026Review
- Decoding glioblastoma evolution and heterogeneity through mechanistic modeling: implications for clinical translation.Journal of experimental & clinical cancer research : CR · 2026Review
- ITM2A promotes thyroid cancer differentiation through metabolic reprogramming and enhances PD-L1-dependent T-cell responses.Clinical and experimental medicine · 2026Article
- IDH1-R132H enhances oncolytic HSV-1 therapy by facilitating viral entry and immune activation in glioma.Nature communications · 2026Article
- JAK-STAT signaling pathway in cancer: from molecular mechanisms to clinical intervention.Molecular cancer · 2026Review
- mRNA vaccine development for tuberculosis: antigen design, immune mechanisms, and translational challenges.Archives of microbiology · 2026Review
- Engineered BCG selectively triggers trained immunity in tumor-associated macrophages and sensitizes glioblastoma to radiotherapy in mice.Nature communications · 2026Article
- Humanized Murine Glioblastoma Models for Evaluation of Coxsackievirus Oncolytic Therapy.Cancers · 2026Article
- Microglial fructose metabolism is essential for glioblastoma growth.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Tumor immunogenicity shapes CNS immune niches and CD8⁺ T cell fate in glioblastoma.Journal of neuroinflammation · 2026Article
- C5aR1 Inhibition Alleviates Cranial Radiation-Induced Cognitive Decline.Cancer research · 2026Article
- Quantitative Cell Type-Specific Immunopeptidome Analysis of Macrophage and Tumor Coevolution Reveals Therapeutic MHC-I Peptides in Glioblastoma.Cancer research · 2025Article
- A Myeloid Cell-Targeted Immunostimulant Cocktail (MyTai) Enhances Cancer Immunotherapy.ACS nano · 2025Article
- Article
- Serial multiomics uncovers anti-glioblastoma responses not evident by routine clinical analyses.Science translational medicine · 2025Article
- Wnt inhibition alleviates resistance to anti-PD1 therapy and improves antitumor immunity in glioblastoma.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Co-mutation of PCLO and SYNE1 defines an immune-activated endometrial cancer subtype with favorable prognosis.The journal of obstetrics and gynaecology research · 2025Article
- Complex I inhibition combined with TLR activation in the breast tumor microenvironment educates cytotoxic neutrophils.Science advances · 2025Article
- Article
- Effect of Photothermal Therapy Using Gold Nanoparticles Conjugated with Hyaluronic Acid in an Intracranial Murine Glioblastoma Model.International journal of nanomedicine · 2025Article
Corrections and comments
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Authors and funding
23 authors at 7 institutions in 1 country.
Funding
Abstract
Background: The GL261 and CT2A syngeneic tumor lines are frequently used as immunocompetent orthotopic mouse models of human glioblastoma (huGBM) but demonstrate distinct differences in their responses to immunotherapy. Methods: To decipher the cell-intrinsic mechanisms that drive immunotherapy resistance in CT2A-luc and to define the aspects of human cancer biology that these lines can best model, we systematically compared their characteristics using whole exome and transcriptome sequencing, and protein analysis through immunohistochemistry, Western blot, flow cytometry, immunopeptidomics, and phosphopeptidomics. Results: The transcriptional profiles of GL261-luc2 and CT2A-luc tumors resembled those of some huGBMs, despite neither line sharing the essential genetic or histologic features of huGBM. Both models exhibited striking hypermutation, with clonal hotspot mutations in RAS genes ( Conclusion: Although the clinical contexts that can be modeled by GL261 and CT2A for huGBM are limited, CT2A may be an informative model of immunotherapy resistance due to its deficits in antigen presentation machinery and interferon response pathways.
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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.