English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 855753      Online Users : 1380
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/3990099045/2665


    Title: Aberrant expression of cell-cycle regulator cyclin DI in breast cancer is related to chromosomal genomic instability
    Authors: Lung, JCY;Chu, JS;Yu, JC;Yue, CT;Lo, YL;Shen, CY;Wu, CW
    Contributors: National Institute of Cancer Research
    Abstract: To account for the accumulation of genomic alterations required for tumor progression, it has been suggested that the genomes of cancer cells are unstable and that this instability results from defective mutators (the "murator phenotype" theory). To examine the hypothesis that abnormal cell-cycle regulators act as the mutators contributing to genomic instability, the present study, based on primary tumor tissues from 71 patients with breast cancer, was performed to determine whether there was an association between aberrant expression of cell-cycle regulators (cyclin A, cyclin D 1, cyclin E, RBI, p21, and p27) and chromosomal instability. Comparative genomic hybridization was used to measure chromosomal changes, reflecting genomic instability in individual tumors, whereas immunohistochemistry was used to detect aberrant expression of cell-cycle regulators. Overexpression of cyclin D I was found to be significantly correlated with increased chromosomal instability (defined as harboring more than 7 chromosomal changes), with 63% of tumors overexpressing and 27% of tumors not overexpressing, with cyclin D I showing chromosomal instability (P < 0.05). Interestingly, this relationship was independent of cell outgrowth (as detected by the proliferation marker Ki-67) and was particularly significant in tumors not expressing p27 or in tumors with detectable RBI. These results suggest that cyclin D I plays an alternative role in the regulation of genomic stability. (C) 2002 Wiley-Liss, Inc.
    Keywords: Oncology;Genetics & Heredity
    Date: 2002-07
    Relation: Genes Chromosomes and Cancer. 2002 Jul;34(3):276-284.
    Link to: http://dx.doi.org/10.1002/gcc.10072
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1045-2257&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000175842700003
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0036107422
    Appears in Collections:[吳成文(1996-2008)] 期刊論文

    Files in This Item:

    File Description SizeFormat
    000175842700003.pdf1759KbAdobe PDF581View/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