AI Article Synopsis
- Patients with ulcerative colitis or Crohn's disease face a heightened risk of colon cancer due to chronic inflammation.
- The paper explores how this inflammation leads to genetic mutations in critical tumor suppressor genes (TP53 and APC), which contribute to cancer development.
- A mathematical model incorporating these genes and related factors illustrates how mutations lead to abnormal cell growth in the colon, providing a basis for future research on early colon cancer stages.
Article Abstract
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-κB, β-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.
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| http://dx.doi.org/10.1016/j.jtbi.2012.09.025 | DOI Listing |
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