1,721,029 research outputs found

    Functional Analysis of Ebv in Nasopharyngeal Carcinoma Cells

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    A membrane invasion culture system was used to study the ability of EBV to enhance invasion and migration of nasopharyngeal carcinoma (NPC) cells. Semi-reverse transcriptase-PCR analysis of matrix proteinases and angiogenic factors from EBV-infected, or EBV-positive (EBV+) , cells demonstrated different degrees of elevated gene expression. In our animal model, EBV+ tumors grew faster and larger than EBV-free, or EBV-negative ( EBV-), tumors and also had clonal EBV terminal repeat sequences. Double- localization of EBV and certain host proteins in EBV+ tumors and biopsy specimens demonstrated that EBV up-regulates host genes only in cells that express those genes but not in cells that do not express them. Double- localization of EBV and host genes in NPC biopsy specimens all showed EBV- tumor cells expressing those host genes. Our data strongly suggest that EBV infection enhances progression of NPC tumor growth. They do not rule out a role for EBV infection in the induction and early promotion of NPC development. Unidentified factors may also enhance NPC tumor growth independent of the effects of EBV

    Synthesis and Antitumor Evaluation of Water-Soluble Derivatives of Glyfoline

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    Three types of water-soluble derivatives of the antitumor agent glyfoline : hydrochloride salts of 6-O-(N,N- dimethylaminoalkyl) glyfoline (Type 1), triethanolamine salts of glyfoline-6-O-alkylcarboxylate (Type 2), and hydrochloride salts of glyfoline-6-O-carbamate (Type 3), were synthesized for evaluation of their antitumor activities. Among these compounds, the triethanolamine salt of 6-O-(3-carboxypropyl)glyfoline (13) showed potent antitumor efficacy in mice bearing nasopharyngeal carcinoma( NPC) xenograft

    Epstein–Barr Virus: New Research in Epithelial Carcinoma

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    Epstein-Barr virus (EBV) can not be detected in untransformed squamous metaplastic epithelia of nasophparynx, but can be detected as an episomal form in certain nasopharyngeal carcinoma (NPC) biopsy specimens and cell lines. In the latter only a subpopulation of NPC cells contains EBV DNA. It appears only in the early passages, but disappears in all lines after 30 passages. EBV can not infect NPC cells and other transformed epithelial cells directly, but can only infect the transformed epithelial cells if the latter express IgA receptor (IgAR) through IgAR mediated endocytosis. EBVinfected (EBV+) NPC cells show clonal terminal repeats of EBV DNA. EBV enhances the proliferation rate, invasion activity and the expressions of some growth factors and their receptors, the cytokines, invasion and metastasis-related genes in vitro. Untransformed squamous metaplastic epithelia of nasopharynx do not express EBV receptor or IgAR. The IgAR expression and EBV infection in severe dysplastic epithelia and carcinoma in situ of nasopharynx are unusual. But about 70 to 80% of tumor cells in each EBV+ NPC case are infected by EBV. The EBV+ NPC cells in the biopsy specimens have a geographical distribution with areas of clonal expansion and some EBV+ lymphocytic infiltration. Each biopsy specimen contains 4 types of NPC cells: tumor cells do not express IgAR and not contain EBV DNA; tumor cells express strong IgAR and contain EBV or not; tumor cells express very weak or no IgAR but contain EBV DNA. The EBV+ xenografts in the SCID mice grow faster and bigger than the EBVgrafts. The EBV+ tumor mass also has a clonal terminal repeats of EBV DNA sequence. In the EBV- NPC xenograft, a fraction of the cells expresses moderate EGFR protein. However, in EBV+ xenograft, some tumor cells contain both EBV signal and strong EGFR protein expression, but other fraction of those tumor cells only contain EBV signal without EGFR protein. The same phenomenon has also presented in the double localization of EBV signal and MDM2 protein. The EBV latent membrane protein (LMP-1) in the NPC cells can not regulated the host gene expression which is not expressed in the host cells, but can indirectly regulated certain host gene expression which are expressed in the host cells. The major function of EBV in infected NPC cells is to enhance tumor cell progression but less likely to play a role as an initiator or promoter in NPC pathogenesis
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