ArticleCell death & disease2025
ULBP2 CAR-T cells enhance gastric cancer immunotherapy by inhibiting CAF activation.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Chimeric Antigen Receptor-Immune Cell-Based Therapies for Clear Cell Renal Cell Carcinoma: Latest Advancements and Directions.Cancers · 2026Review
- Organ-Specific Migration License (OSML) theory: a novel paradigm for spatiotemporal regulation and intervention of cross-organ immune cell migration in tumor immune responses.Cell communication and signaling : CCS · 2026Review
- Multi-omics analysis and experimental validation uncovers prognosis significance of IKBIP in patients with hepatocellular carcinoma: a multicenter cohort study.BMC gastroenterology · 2026Article
- The research advances of crosstalk between cancer-associated fibroblasts and tumor cells using co-culture organoids.Cell death & disease · 2026Review
- Patient-derived organoids in gastric cancer: bridging the tumor microenvironment to functional precision oncology.Frontiers in bioengineering and biotechnology · 2026Review
- NKG2D CAR-T cells for solid tumor immunotherapy: advances, challenges, and future directions.Frontiers in immunology · 2026Review
- Association Between Amino Acid Polymorphisms in MICA and MICA-NKG2D Interaction Affinity: Implications and Significance for Tumor Immunity.Biomolecules · 2025Review
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Gastric cancer (GC) is characterised by a dense stromal microenvironment, lack of therapeutic targets, and limited effective treatment options, collectively leading to a poor prognosis. Here, we identify UL16 binding protein 2 (ULBP2) as a potential therapeutic target in GC. Mechanistically, ULBP2 overexpression activates the TGF-β signalling pathway, promoting the activation of cancer-associated fibroblasts (CAFs) and tumor progression in GC. Furthermore, we developed ULBP2 CAR-T cells and assessed their therapeutic potential in GC cell lines, organoids, cell line-derived xenograft (CDX) and patient-derived xenograft (PDX) mouse models. We showed that ULBP2 CAR-T cells effectively eliminated GC cell lines and organoids and, either alone or in combination with an anti-PD-1 antibody, significantly inhibited tumor growth and prolonged survival in both CDX and PDX mouse models. In conclusion, ULBP2 contributes to GC progression by promoting TGF-β mediated CAF activation, which collectively reinforce the dense stromal microenvironment. Targeting ULBP2 suppresses tumor growth, reduces stromal deposition, and promotes T cell infiltration, thereby enhancing the efficacy of immunotherapy in GC.
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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.