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Epstein-Barr virus and gastric carcinoma.

Abstract

The Epstein-Barr virus (EBV) is detected in the tissue of about 10% of gastric carcinoma cases throughout the world. In each case, 100% of carcinoma cells are infected with EBV. Analysis of EBV in carcinoma biopsies indicates that carcinoma is formed by the proliferation of a single EBV infected cell. These findings suggest that EBV plays an important role in the development of EBV positive gastric carcinomas. The EBV genes expressed are EBV determined nuclear antigen 1 (EBNA1), two small non-polyadenylated RNAs known as EBER1 and EBER2, and the transcripts from the BamHI-A region (BARF0); in addition, some cases also express a small amount of latent membrane protein 2A (LMP2A). Epithelial cells are refractory to EBV infection in vitro. This has hampered the study of the role of EBV in epithelial malignancies. The use of recombinant EBV carrying a selectable marker has enabled this difficulty to be overcome. EBV infected cell clones can be obtained from most carcinoma cell lines examined, and it was found that cell to cell contact was an efficient mode of EBV infection. Furthermore, it was possible to immortalize primary gastric epithelial cells by EBV infection. The cells expressed identical EBV genes to those typically seen in EBV positive gastric carcinoma, and showed accelerated malignant properties, including growth in soft agarose and tumorigenicity in severe combined immunodeficient (SCID) mice. These results suggest that EBV contributes to the maintenance of the malignant phenotype of EBV positive gastric carcinoma.

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  • Authors+Show Affiliations

    Department of Tumor Virology, Hokkaido University, Sapporo, Japan. kentaka@med.hokudai.ac.jp

    Source

    Molecular pathology : MP 53:5 2000 Oct pg 255-61

    MeSH

    Animals
    Biomarkers
    Cell Division
    Cell Transformation, Viral
    Epithelial Cells
    Gene Expression
    Genes, Viral
    Herpesviridae Infections
    Herpesvirus 4, Human
    Humans
    Membrane Proteins
    Mice
    Mice, SCID
    Oncogenic Viruses
    RNA, Viral
    Stomach Neoplasms
    Tumor Cells, Cultured
    Tumor Virus Infections

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    11091849

    Citation

    Takada, K. "Epstein-Barr Virus and Gastric Carcinoma." Molecular Pathology : MP, vol. 53, no. 5, 2000, pp. 255-61.
    Takada K. Epstein-Barr virus and gastric carcinoma. MP, Mol Pathol. 2000;53(5):255-61.
    Takada, K. (2000). Epstein-Barr virus and gastric carcinoma. Molecular Pathology : MP, 53(5), pp. 255-61.
    Takada K. Epstein-Barr Virus and Gastric Carcinoma. MP, Mol Pathol. 2000;53(5):255-61. PubMed PMID: 11091849.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Epstein-Barr virus and gastric carcinoma. A1 - Takada,K, PY - 2000/11/25/pubmed PY - 2001/2/28/medline PY - 2000/11/25/entrez SP - 255 EP - 61 JF - Molecular pathology : MP JO - MP, Mol. Pathol. VL - 53 IS - 5 N2 - The Epstein-Barr virus (EBV) is detected in the tissue of about 10% of gastric carcinoma cases throughout the world. In each case, 100% of carcinoma cells are infected with EBV. Analysis of EBV in carcinoma biopsies indicates that carcinoma is formed by the proliferation of a single EBV infected cell. These findings suggest that EBV plays an important role in the development of EBV positive gastric carcinomas. The EBV genes expressed are EBV determined nuclear antigen 1 (EBNA1), two small non-polyadenylated RNAs known as EBER1 and EBER2, and the transcripts from the BamHI-A region (BARF0); in addition, some cases also express a small amount of latent membrane protein 2A (LMP2A). Epithelial cells are refractory to EBV infection in vitro. This has hampered the study of the role of EBV in epithelial malignancies. The use of recombinant EBV carrying a selectable marker has enabled this difficulty to be overcome. EBV infected cell clones can be obtained from most carcinoma cell lines examined, and it was found that cell to cell contact was an efficient mode of EBV infection. Furthermore, it was possible to immortalize primary gastric epithelial cells by EBV infection. The cells expressed identical EBV genes to those typically seen in EBV positive gastric carcinoma, and showed accelerated malignant properties, including growth in soft agarose and tumorigenicity in severe combined immunodeficient (SCID) mice. These results suggest that EBV contributes to the maintenance of the malignant phenotype of EBV positive gastric carcinoma. SN - 1366-8714 UR - https://www.unboundmedicine.com/medline/citation/11091849/full_citation L2 - http://mp.bmj.com/cgi/pmidlookup?view=long&pmid=11091849 DB - PRIME DP - Unbound Medicine ER -