ArticleJournal for immunotherapy of cancer2024
Immune microenvironment of Epstein-Barr virus (EBV)-negative compared to EBV-associated gastric cancers: implications for immunotherapy.
Article in Journal for immunotherapy of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- The deubiquitinating enzyme USP42 promotes lung adenocarcinoma progression through PTGS2.Journal of molecular histology · 2026Article
- Review
- From Tumor Biology to Clinical Perspectives: Novel Biomarkers and Therapeutic Insights in Gastric Cancer.Oncology research · 2026Review
- Interplay between pathogen-mediated immune evasion and innate immune negative regulation in gastrointestinal tumors.Frontiers in immunology · 2026Review
- Integrated Bulk and Single-Cell Transcriptomic Analyses Identify a Five-Gene Signature Associated With Prognosis and the Tumor Microenvironment in Epstein-Barr Virus-Associated Gastric Cancer.Genetics research · 2026Article
- Molecular Mechanisms and Biomarkers Driving the Transition From Chronic Atrophic Gastritis to Gastric Cancer.Clinical Medicine Insights. Oncology · 2026Review
- Immune checkpoint inhibitors in infectious diseases: therapeutic reinvigoration, immunopathology, and precision targeting.Frontiers in immunology · 2026Review
- Epstein-Barr virus infection shapes the genetic, transcriptomic, and immune microenvironment landscape of Burkitt lymphoma.Infectious agents and cancer · 2025Article
- Immune-mediated bone loss: A Mendelian randomization and NHANES-based study of viral infections and osteoporosis.Virus research · 2025Article
- Microbiome meets immunotherapy: unlocking the hidden predictors of immune checkpoint inhibitors.NPJ biofilms and microbiomes · 2025Article
- Platelets in cancer and immunotherapy: functional dynamics and therapeutic opportunities.Experimental hematology & oncology · 2025Review
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Abstract
backgroundGastric carcinomas (GC) are aggressive malignancies, and only ~15% of patients respond to anti-programmed cell death (ligand) 1 (PD-(L)1) monotherapy. However, Epstein-Barr virus (EBV)-associated GCs (~5-10% of GCs) often harbor PD-L1 and PD-L2 chromosomal amplifications and robust CD8+ T cell infiltrates, and respond at a high rate to anti-PD-1. The current study compares the tumor immune microenvironments (TiMEs) of EBV+ versus EBV(-) GCs.
methodsOver 1000 cases of primary invasive GCs were screened to identify 25 treatment-naïve specimens for study (11 EBV+, 14 EBV(-)). Quantitative immunohistochemistry (IHC) was conducted for markers of immune cell subsets and co-regulatory molecules. Gene expression profiling (GEP) was performed on RNAs isolated from macrodissected areas of CD3+ T cell infiltrates abutting PD-L1+ stromal/tumor cells, using multiplex quantitative reverse transcriptase PCR for a panel of 122 candidate immune-related genes.
resultsIHC revealed that 17/25 GCs contained PD-L1+ stromal cells, with no significant difference between EBV+/- specimens; however, only 3/25 specimens (all EBV+) contained PD-L1+ tumor cells. CD8+ T cell densities were higher in EBV+ versus EBV(-) tumors (p=0.044). With GEP normalized to the pan-leukocyte marker
conclusionsWhile certain markers of immunosuppression are found in the GC TiME regardless of EBV status, EBV(-) GCs, which are much more common than EBV+ GCs, overexpress components of the COX-2/PGE2 pathway. These findings provide novel insights into the immune microenvironments of EBV+ and EBV(-) GC, and offer potential targets to overcome resistance to anti-PD-(L)1 therapies.
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