ASIA unversity:Item 310904400/4629
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 90587/105803 (86%)
造訪人次 : 16865719      線上人數 : 81
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜尋範圍 查詢小技巧:
  • 您可在西文檢索詞彙前後加上"雙引號",以獲取較精準的檢索結果
  • 若欲以作者姓名搜尋,建議至進階搜尋限定作者欄位,可獲得較完整資料
  • 進階搜尋


    題名: P27kip1 down-regulation is associated with trastuzumab resistance in breast cancer cells
    作者: Nahta, R.;Takahahshi, T.;Ueno, N. T.;Mien-Chie Hung;Esteva, F. J.
    日期: 2004-06
    上傳時間: 2009-11-27 13:57:08 (UTC+8)
    出版者: Asia University
    摘要: Trastuzumab (Herceptin) is a recombinant humanized monoclonal antibody directed against HER-2. The objective response rate to trastuzumab monotherapy is 12?34% for a median duration of 9 months, by which point most patients become resistant to treatment. We created two trastuzumab-resistant (TR) pools from the SKBR3 HER-2-overexpressing breast cancer cell line to study the mechanisms by which breast cancer cells escape trastuzumab-mediated growth inhibition. Both pools maintained her-2 gene amplification and protein overexpression. Resistant cells demonstrated a higher S-phase fraction by flow cytometry and a faster doubling time of 24?36 h compared with 72 h for parental cells. The cyclin-dependent kinase inhibitor p27kip1 was decreased in TR cells, and cyclin-dependent kinase 2 activity was increased. Importantly, exogenous addition of p27kip1 increased trastuzumab sensitivity. Additionally, resistant cells displayed heightened sensitivity to the proteasome inhibitor MG132, which induced p27kip1 expression. Thus, we propose that trastuzumab resistance may be associated with decreased p27kip1 levels and may be susceptible to treatments that induce p27kip1 expression.
    關聯: CANCER RESEARCH 64(-):3981-3986
    顯示於類別:[生物科技學系] 期刊論文


    檔案 描述 大小格式瀏覽次數
    310904400-4629.doc34KbMicrosoft Word434檢視/開啟


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