English  |  正體中文  |  简体中文  |  Items with full text/Total items : 51510/86705 (59%)
Visitors : 8274964      Online Users : 95
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library & TKU 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://tkuir.lib.tku.edu.tw:8080/dspace/handle/987654321/80398

    Title: Mathematical model of heterogeneous cancer growth with an autocrine signalling pathway
    Authors: Hu, G.-M.;Lee, C.-Y.;Chen, Y.-Y.;Pang, N.-N.;Tzeng, W. J.
    Contributors: 淡江大學物理學系
    Date: 2012-10
    Issue Date: 2013-01-23 16:30:32 (UTC+8)
    Publisher: Chichester: Wiley-Blackwell Publishing Ltd.
    Abstract: Objectives
    Cancer is a complex biological occurrence which is difficult to describe clearly and explain its growth development. As such, novel concepts, such as of heterogeneity and signalling pathways, grow exponentially and many mathematical models accommodating the latest knowledge have been proposed. Here, we present a simple mathematical model that exhibits many characteristics of experimental data, using prostate carcinoma cell spheroids under treatment.

    Materials and methods
    We have modelled cancer as a two-subpopulation system, with one subpopulation representing a cancer stem cell state, and the other a normal cancer cell state. As a first approximation, these follow a logistical growth model with self and competing capacities, but they can transform into each other by using an autocrine signalling pathway.

    Results and conclusion
    By analysing regulation behaviour of each of the system parameters, we show that the model exhibits many characteristics of actual cancer growth curves. Features reproduced in this model include delayed phase of evolving cancer under 17AAG treatment, and bi-stable behaviour under treatment by irradiation. In addition, our interpretation of the system parameters corresponds well with known facts involving 17AAG treatment. This model may thus provide insight into some of the mechanisms behind cancer.
    Relation: Cell Proliferation 45(5), pp.445-455
    DOI: 10.1111/j.1365-2184.2012.00835.x
    Appears in Collections:[物理學系暨研究所] 期刊論文

    Files in This Item:

    File Description SizeFormat
    Hu12.pdf1337KbAdobe PDF269View/Open

    All items in 機構典藏 are protected by copyright, with all rights reserved.

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