Mathematical model of colitis-associated colon cancer

被引：4
|
作者：
Lo, Wing-Cheong [1 ]
Martin, Edward W., Jr. [2 ,3 ,4 ]
Hitchcock, Charles L. [5 ]
Friedman, Avner [1 ,6 ]
机构：
[1] Ohio State Univ, Math Biosci Inst, Columbus, OH 43210 USA
[2] Ohio State Univ, Arthur G James Canc Hosp, Dept Surg, Div Surg Oncol, Columbus, OH 43210 USA
[3] Ohio State Univ, Richard J Solove Res Inst, Columbus, OH 43210 USA
[4] Ohio State Univ, Ctr Comprehens Canc, Columbus, OH 43210 USA
[5] Ohio State Univ, Dept Pathol, Columbus, OH 43210 USA
[6] Ohio State Univ, Dept Math, Columbus, OH 43210 USA
来源：
JOURNAL OF THEORETICAL BIOLOGY | 2013年 / 317卷
基金：
美国国家科学基金会;
关键词：
Colorectal cancer; Mucin; APC; TP53; Mathematical model; NF-KAPPA-B; BETA-CATENIN; ALTERED DISTRIBUTION; COLORECTAL-CANCER; BINDING-PROTEINS; MUCIN DYNAMICS; GENE; APC; ACTIVATION; INFLAMMATION;
D O I：
10.1016/j.jtbi.2012.09.025
中图分类号：
Q [生物科学];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
As a result of chronic inflammation of their colon, patients with ulcerative colitis or Crohn's disease are at risk of developing colon cancer. In this paper, we consider the progression of colitis-associated colon cancer. Unlike normal colon mucosa, the inflammed colon mucosa undergoes genetic mutations, affecting, in particular, tumor suppressors TP53 and adenomatous polyposis coli (APC) gene. We develop a mathematical model that involves these genes, under chronic inflammation, as well as NF-kappa B, beta-catenin, MUC1 and MUC2. The model demonstrates that increased level of cells with TP53 mutations results in abnormal growth and proliferation of the epithelium; further increase in the epithelium proliferation results from additional APC mutations. The model may serve as a conceptual framework for further data-based study of the early stage of colon cancer. (C) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码：20 / 29
页数：10
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