simplified tumour model established via Epstein-Barr virus-encoded, nasopharyngeal carcinoma-derived oncogene latent membrane protein 1 in immunocompetent mice
The expression and immune modulation of Epstein-Barr virus-encoded oncogene latent membrane protein 1 (N-LMP1) is essential in the pathogenesis of nasopharyngeal carcinoma. In previous studies, cell transformation has been induced by the expression of EBV-encoded N-LMP1 in non-tumour BALB/c-3T3 cell...
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Published in | Laboratory animals (London) Vol. 42; no. 2; pp. 193 - 203 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
London, England
SAGE Publications
01.04.2008
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Subjects | |
Online Access | Get full text |
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Summary: | The expression and immune modulation of Epstein-Barr virus-encoded oncogene latent membrane protein 1 (N-LMP1) is essential in the pathogenesis of nasopharyngeal carcinoma. In previous studies, cell transformation has been induced by the expression of EBV-encoded N-LMP1 in non-tumour BALB/c-3T3 cells and these cells have then been used to form tumours in T-cell-deficient nude mice. However, studies using this model have been limited by the lack of a competent immune system. To facilitate the study of immune components in N-LMP1-driven oncogenesis, we herein developed a simplified N-LMP1-derived tumour model in immunocompetent mice. Cell transformation was induced by the expression of N-LMP1 in BALB/c-3T3 cells, and these transformants were used to induce oncogenesis in BALB/c mice. In contrast to the 100% successful tumour-induction rate in nude mice treated with monodispersed transformed cells, the tumour incidence in BALB/c mice was only 5-36%. However, the transplantation of tumour fragments into BALB/c mice yielded a reproducible tumour-induction rate of >85%, which is acceptable for most of the research needs. This novel model of N-LMP1-directed oncogenesis in an immunocompetent environment may serve as an important platform for the future assessment of N-LMP1-targeted tumour therapies. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0023-6772 1758-1117 |
DOI: | 10.1258/la.2007.006037 |