中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/47712
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 29490/55136 (53%)
Visitors : 1997935      Online Users : 315
RC Version 7.0 © 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.cmu.edu.tw/ir/handle/310903500/47712


    Title: 非同源末梢黏合DNA修補系統與口腔癌化關聯之探究
    http://grbsearch.stpi.narl.org.tw/GRB/result.jsp?id=1902528&plan_no=NSC98-2320-B039-010-MY3&plan_year=98&projkey=PC9808-0475&target=plan
    Authors: 包大?(Da-Tian Bau);蔡銘修(Ming-Hsui Tsai)
    Contributors: 醫學院臨床醫學研究所;中國附醫醫研部泰瑞法克斯癌症研究實驗室
    Date: 2011-07-31
    Issue Date: 2013-01-25 15:30:52 (UTC+8)
    Abstract: Oral cancer is ranked the forth leading cause of cancer incidence among Taiwanese male population. It is believed that in addition to environmental factors, such as smoking, alcohol drinking, and betel quid chewing, the subtle deficiencies of DNA repair systems, caretakers care of the genome, maybe also related to oral carcinogenesis. Therefore, the systematic understanding of the genotypes and the phenotypes of these DNA repair genes will help us to reveal the oral carcinogenesis progression. The direct or indirect intracellular effects of exposures to smoking, alcohol drinking, and betel quid chewing can cause DNA damages, including double strand breaks. A loss or delay in repairing these double strand breaks on time may cause a dramatically instable of the genome. Thus, a subtle variation in the capacity of double strand break repair may be related to oral carcinogenesis. Recently, we have indeed found that the genetic polymorphic variations of XRCC4, a member of the important system for DNA double strand break repair, non-homologous end-joining (NHEJ), are associated with oral cancer susceptibility. Thus in this 3-year project, we aim toelucidate the contribution of NHEJ to oral carcinogenesis via three levels including human population, cell model, and animal model, respectively. In the first year, 2009-2010, we have investigated some important candidate variant single nucleotide polymorphisms in three of NHEJ genes, and evaluated the associations between these polymorphisms and oral cancer risk. By the way, the effects of gene-gene interactions, and the environmental factors have be combined with these genetic factors to evaluate their combined contribution to oral cancer etiology. We have published several SCI papers in journals such as Laryngoscope, Oral Oncology, Anticancer Research, etc.In the current year, more than we have planned, we have established several oral cancer primary cell lines from the oral cancer patients, and to compare them with those normal cells. We are now examining their differences in phenotypes such as in vitro and in vivo NHEJ and overall double strand break repair capacities investigated. By the way, the differential expression patterns between cancer and normal cells of the NHEJ proteins will be examined by Northern and Western Blotting, separately. Also, we have being prepared the animal model for the third year.
    Appears in Collections:[Graduate Institute of Clinical Medical Science] Research reports

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML155View/Open


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

     


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