ArticleGut2023
Multivalent tyrosine kinase inhibition promotes T cell recruitment to immune-desert gastric cancers by restricting epithelial-mesenchymal transition via tumour-intrinsic IFN-γ signalling.
Article in Gut, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting receptor tyrosine kinases: from molecular mechanisms to clinical therapeutics.Signal transduction and targeted therapy · 2026Review
- Review
- Deciphering IFN signaling in gastric cancer: A single-cell and bulk transcriptomic integration reveals CXCR4 as a key immunomodulator and prognostic determinant.Translational oncology · 2026Article
- Advances in the molecular subtyping of gastric cancer.World journal of surgical oncology · 2026Review
- Dynamic systemic immune-inflammation index predicts survival after neoadjuvant immunotherapy in gastric cancer: A multicenter study.iScience · 2026Article
- MOncogene · 2026Article
- Single-cell and spatial transcriptome analysis reveals the potential therapeutic targets for testicular sex cord-stromal cell tumor.Biomarker research · 2026Article
- TiRank prioritizes phenotypic niches in tumor microenvironment for clinical biomarker discovery.Genome medicine · 2026Article
- Tumor microenvironment dynamics in gastric cancer pathogenesis and therapeutic resistance.Molecular cancer · 2026Review
- GULP1 Fuels Resistance to PD-1 Blockade through Lipid-Mediated Metabolic Reprogramming of Tumor-Associated Macrophages in Gastric Cancer.Cancer communications (London, England) · 2026Article
- Integrative Multi-Omics Analysis Uncovers Immunological Phenotypes Predictive of Combinatorial Immunotherapy Response in Gastric Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TREM2 facilitates gastric cancer progression and immune evasion via inhibiting TRIM21-mediated STAT1 degradation in tumor-associated macrophages.Cell death & disease · 2025Article
- Repurposing the Tyrosine Kinase Inhibitors Targeting FGFR and VEGFR Pathways for Cancer Therapy: A Comprehensive Review.Cancers · 2025Review
- Bifidobacterium boosts anti-PD-1 effectiveness through JAK pathway in hepatocellular carcinoma.NPJ precision oncology · 2025Article
- Systematic benchmarking of large Language models in programmed cell death-oriented gastric cancer research: a comparative analysis of DeepSeek‑V3, DeepSeek‑R1, and Claude 3.5.Discover oncology · 2025Article
- Combining Apatinib and Oxaliplatin Remodels the Immunosuppressive Tumor Microenvironment and Sensitizes Desert-Type Gastric Cancer to Immunotherapy.Cancer research · 2025Article
- Blockade of CLEVER-1 restrains immune evasion and enhances anti-PD-1 immunotherapy in gastric cancer.Journal for immunotherapy of cancer · 2025Article
- Overcoming immunotherapy resistance in gastric cancer: insights into mechanisms and emerging strategies.Cell death & disease · 2025Review
- FDA-approved drug repurposing screen identifies inhibitors of SARS-CoV-2 pseudovirus entry.Frontiers in pharmacology · 2025Article
- Inflammatory factors collaboratively linkFrontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
19 authors at 3 institutions in 3 countries.
Funding
Abstract
objectiveGastric cancer (GC) ranks fifth in incidence and fourth for mortality worldwide. The response to immune checkpoint blockade (ICB) therapy in GC is heterogeneous due to tumour-intrinsic and acquired immunotherapy resistance. We developed an immunophenotype-based subtyping of human GC based on immune cells infiltration to develop a novel treatment option.
designA algorithm was developed to reclassify GC into immune inflamed, excluded and desert subtypes. Bioinformatics, human and mouse GC cell lines, syngeneic murine gastric tumour model, and CTLA4 blockade were used to investigate the immunotherapeutic effects by restricting receptor tyrosine kinase (RTK) signalling in immune desert (ICB-resistant) type GC.
resultsOur algorithm restratified subtypes of human GC in public databases and showed that immune desert-type and excluded-type tumours are ICB-resistant compared with immune-inflamed GC. Moreover, epithelial-mesenchymal transition (EMT) signalling was highly enriched in immune desert-type GC, and syngeneic murine tumours exhibiting mesenchymal-like, compared with epithelial-like, properties are T cell-excluded and resistant to CTLA4 blockade. Our analysis further identified a panel of RTKs as potential druggable targets in the immune desert-type GC. Dovitinib, an inhibitor of multiple RTKs, strikingly repressed EMT programming in mesenchymal-like immune desert syngeneic GC models. Dovitinib activated the tumour-intrinsic SNAI1/2-IFN-γ signalling axis and impeded the EMT programme, converting immune desert-type tumours to immune inflamed-type tumours, sensitising these mesenchymal-like 'cold' tumours to CTLA4 blockade.
conclusionOur findings identified potential druggable targets relevant to patient groups, especially for refractory immune desert-type/ 'cold' GC. Dovitinib, an RTK inhibitor, sensitised desert-type immune-cold GC to CTLA4 blockade by restricting EMT and recruiting T cells.
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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.