國家衛生研究院 NHRI:Item 3990099045/3104
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 911305      Online Users : 900
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/3104


    Title: Amplicons on chromosome 3 contain oncogenes induced by recurrent exposure to 12-O-tetradecanoylphorbol-13-acetate and sodium n-butyrate and Epstein-Barr virus reactivation in a nasopharyngeal carcinoma cell line
    Authors: Lee, CH;Fang, CY;Sheu, JJC;Chang, Y;Takada, K;Chen, JY
    Contributors: Division of Clinical Research;National Institute of Cancer Research
    Abstract: Nasopharyngeal carcinoma (NPC) is closely associated with Epstein-Barr virus (EBV) infection and exposure to environmental carcinogens. In this study, an inducible Epstein-Barr virus (EBV) reactivation NPC cell line, NA, was used to investigate the impact of recurrent 12-O-tetradecanoylphorbol-13-acetate-sodium n-butyrate (TPA/SB) treatment and EBV reactivation on chromosomal abnormalities utilizing array-based comparative genomic hybridization (CGH). It was observed that most copy-number aberrations (CNA) were progressively nonrandomly clustered on chromosomes 3, 8, and 9, as the frequency of TPA/SB treatment and EBV reactivation increased. All of the prominent amplicons detected (including 3p14.1, 3p13, 3p12.3, 3p12.2, 3q26.2, 3q26.31, and 3q26.32) were located on chromosome 3, with multiple oncogenes assigned to these sites. The amplification patterns of 3p 12.3 and 3q26.2 were validated using fluorescence in situ hybridization (FISH) analysis. Subsequent quantitative real-time polymerase chain reaction detected increasing expression of ROBO1 and SKIL oncogenes in NA cells harboring higher frequency of TPA/SB treatment and EBV reactivation, consistent with copy-number amplification of these loci. These findings demonstrate that a high incidence of TPA/SB induced-EBV reactivation has a profound influence on the carcinogenesis of NPC through altered DNA copy number.
    Keywords: Oncology;Genetics & Heredity
    Date: 2008-08
    Relation: Cancer Genetics and Cytogenetics. 2008 Aug;185(1):1-10.
    Link to: http://dx.doi.org/10.1016/j.cancergencyto.2008.03.014
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000258420900001
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=47749124917
    Appears in Collections:[Yao Chang] Periodical Articles
    [Jen-Yang Chen] Periodical Articles
    [Chia-Huei Lee] Periodical Articles

    Files in This Item:

    File Description SizeFormat
    000258420900001.pdf1509KbAdobe PDF1128View/Open


    All items in NHRI are protected by copyright, with all rights reserved.

    Related Items in TAIR

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback