ArticleJournal of virus eradication2025
2-Deoxyglucose as a therapeutic strategy for EBV-associated gastric carcinoma: Glycolytic and lytic reactivation inhibition under hypoxic conditions.
Article in Journal of virus eradication, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Targeting the remodeled peritoneal ecosystem: a paradigm shift from tumor cells to the microenvironment in gastric cancer peritoneal metastasis.Frontiers in immunology · 2026Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epstein-Barr virus-associated gastric carcinoma (EBVaGC), a distinct subtype of gastric cancer, accounts for approximately 10 % of all gastric cancer cases. 2-deoxyglucose (2-DG), a glycolysis inhibitor, has emerged as a crucial tool in cancer therapy. However, the differential effects of 2-DG on EBVaGC and EBV-negative gastric carcinoma (EBVnGC) are not yet fully understood. In this study, we demonstrated that 2-DG inhibited the proliferation of both AGS and AGS-EBV cells, with AGS-EBV cells exhibiting greater sensitivity, particularly under hypoxic conditions. Furthermore, EBV infection was found to upregulate glycolytic gene expression in AGS-EBV cells, particularly under hypoxic conditions, through HIF-1α-dependent mechanisms. Notably, 2-DG also inhibited EBV lytic reactivation in AGS-EBV cells under hypoxic conditions. These findings provide valuable insights into the molecular mechanisms of EBV-mediated metabolic reprogramming and highlight the potential of 2-DG as a therapeutic agent for EBVaGC.
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