ArticleEMBO molecular medicine2024
Immunotherapies targeting the oncogenic fusion gene CLDN18-ARHGAP in gastric cancer.
Article in EMBO molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Claudin18.2 and the PD-1/PD-L1 axis in gastric cancer: mechanistic insights and implications for combination immunotherapy.Journal of translational medicine · 2026Review
- Characterization of Microplastics in Human Gastric Cancer and Control Tissues and Analysis of Associated Genetic Features.Advanced healthcare materials · 2026Article
- Systematic optimization of PD-L1 and CLDN18.2 CAR-T designs identifies a bicistronic dual-target, double-CD3ζ architecture with enhanced antitumor activity in gastric cancer.Frontiers in immunology · 2026Article
- Novel Claudin18.2-Targeted Therapies in Gastrointestinal Tumors.ACS omega · 2025Review
- Harnessing technologies to unravel gastric cancer heterogeneity.Trends in cancer · 2025Review
- Computation strategies and clinical applications in neoantigen discovery towards precision cancer immunotherapy.Biomarker research · 2025Review
- Predictive biomarkers in the era of immunotherapy for gastric cancer: current achievements and future perspectives.Frontiers in immunology · 2025Review
- Multimodal therapeutic strategies against gastric cancer: from conventional treatments to tumor microenvironment targeting.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
The CLDN18-ARHGAP fusion gene is an oncogenic driver newly discovered in gastric cancer. It was detected in 9% (8/87) of gastric cancer patients in our center. An immunogenic peptide specifically targeting CLDN18-ARHGAP fusion gene was generated to induce neoantigen-reactive T cells, which was proved to have specific and robust anti-tumor capacity both in in vitro coculture models and in vivo xenograft gastric cancer models. Apart from the immunogenic potential, CLDN18-ARHGAP fusion gene was also found to contribute to immune suppression by inducing a regulatory T (Treg) cell-enriched microenvironment. Mechanistically, gastric cancer cells with CLDN18-ARHGAP fusion activate PI3K/AKT-mTOR-FAS signaling, which enhances free fatty acid production of gastric cancer cells to favor the survival of Treg cells. Furthermore, PI3K inhibition could effectively reverse Treg cells upregulation to enhance anti-tumor cytotoxicity of neoantigen-reactive T cells in vitro and reduce tumor growth in the xenograft gastric cancer model. Our study identified the CLDN18-ARHGAP fusion gene as a critical source of immunogenic neoepitopes, a key regulator of the tumor immune microenvironment, and immunotherapeutic applications specific to this oncogenic fusion.
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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.