ArticleMolecules and cells2011
Association between Epstein-Barr virus infection and chemoresistance to docetaxel in gastric carcinoma.
Article in Molecules and cells, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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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
26 citing papers in PubMed, 33 citations in OpenAlex.
- Epstein-Barr Virus-Mediated Apoptosis Evasion in Epithelial Malignancies: Molecular Mechanisms and Therapeutic Implications.Biology · 2026Review
- The mycobiome, virome and archaeome in gastrointestinal cancers: molecular pathogenesis and therapeutic intervention.Molecular cancer · 2026Review
- Epstein-Barr Virus Silences GSDME and Pyroptosis in Gastric Cancer.Microorganisms · 2025Article
- Targeting archetypes of viral-driven cancers with immunotherapy: a perspective on immunogenicity within the tumor microenvironment.Frontiers in immunology · 2025Review
- Unlocking the Potential: Epstein-Barr Virus (EBV) in Gastric Cancer and Future Treatment Prospects, a Literature Review.Pathogens (Basel, Switzerland) · 2024Review
- The viral etiology of EBV-associated gastric cancers contributes to their unique pathology, clinical outcomes, treatment responses and immune landscape.Frontiers in immunology · 2024Review
- Article
- Predicting cancer prognosis and drug response from the tumor microbiome.Nature communications · 2022Article
- Cisplatin Resistance in Epstein-Barr-Virus-Associated Gastric Carcinoma Acquired throughCancers · 2021Article
- Article
- Epstein-Barr Virus miR-BART17-5p Promotes Migration and Anchorage-Independent Growth by Targeting Kruppel-Like Factor 2 in Gastric Cancer.Microorganisms · 2020Article
- Methylation of drug resistance-related genes in chemotherapy-sensitive Epstein-Barr virus-associated gastric cancer.FEBS open bio · 2020Article
- Epstein-Barr virus miR-BART1-3p suppresses apoptosis and promotes migration of gastric carcinoma cells by targeting DAB2.International journal of biological sciences · 2020Article
- Review
- Regulation of proliferation and invasion by the IGF signalling pathway in Epstein-Barr virus-positive gastric cancer.Journal of cellular and molecular medicine · 2018Article
- The Predictive Value of Epstein-Barr Virus-Positivity in Patients Undergoing Gastrectomy Followed by Adjuvant Chemotherapy.Chonnam medical journal · 2018Article
- Outlooks on Epstein-Barr virus associated gastric cancer.Cancer treatment reviews · 2018Review
- Long-Term Survival of Patient with Epstein-Barr Virus-Positive Gastric Cancer Treated with Chemotherapy: Case Report.Journal of gastrointestinal cancer · 2016Article
- Epstein-Barr Virus MicroRNA miR-BART20-5p Suppresses Lytic Induction by Inhibiting BAD-Mediated caspase-3-Dependent Apoptosis.Journal of virology · 2016Article
- MicroRNA miR-BART20-5p stabilizes Epstein-Barr virus latency by directly targeting BZLF1 and BRLF1.Journal of virology · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epstein-Barr virus (EBV) is associated with human cancers such as nasopharyngeal carcinoma, Burkitt's lymphoma, Hodgkin's disease, and gastric carcinoma (GC). EBV is associated with about 10% of all GC cases globally. EBV-associated GC has distinct features from EBV-negative GC. However, it is still unclear if EBV infection has any effect on GC chemoresistance. Cell proliferation assay, cell cycle analysis, and active caspase Western blot revealed that the EBV-positive GC cell line (AGS-EBV) showed chemoresistance to docetaxel compared to the EBV-negative GC cell line (AGS). Docetaxel treatment increased expression of Bax similarly in AGS and AGS-EBV cell lines. However, Bcl-2 induction was markedly higher in AGS-EBV cells, after docetaxel treatment. Although docetaxel increased the expression of p53 to a similar extent in both cell lines, induction of p21 in AGS-EBV cells was lower than in AGS cells. Furthermore, expression of survivin was higher in AGS-EBV cells than in AGS cells following docetaxel treatment as well as at basal state. EBVlytic gene expression was induced by docetaxel treatment in AGS-EBV cells. The results suggest that EBV infection and lytic induction confers chemoresistance to GC, possibly by regulating cellular and EBV latent and lytic gene expression.
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Registered trials
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