%0 Journal Article
%T Development of an Inflammation-Associated Colorectal Cancer Model and Its Application for Research on Carcinogenesis and Chemoprevention
%A Takuji Tanaka
%J International Journal of Inflammation
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/658786
%X Chronic inflammation is a well-recognized risk factor for development of human cancer in several tissues, including large bowel. Inflammatory bowel disease, including ulcerative colitis and Crohn¡¯s disease, is a longstanding inflammatory disease of intestine with increased risk for colorectal cancer development. Several molecular events involved in chronic inflammatory process may contribute to multistep carcinogenesis of human colorectal cancer in the inflamed colon. They include overproduction of reactive oxygen and nitrogen species, overproduction and upregulation of productions and enzymes of arachidonic acid biosynthesis pathway and cytokines, and intestinal immune system dysfunction. In this paper, I will describe several methods to induce colorectal neoplasm in the inflamed colon. First, I will introduce a protocol of a novel inflammation-associated colon carcinogenesis in mice. In addition, powerful tumor-promotion/progression activity of dextran sodium sulfate in the large bowel of mice will be described. Finally, chemoprevention of inflammation-associated colon carcinogenesis will be mentioned. 1. Introduction Relationship between inflammation and cancer has been suggested for a long time [1]. Since Marshall and Warren [2], who discovered Helicobacter pylori and reported its infection closely associated with gastric cancer development, won the Nobel Prize in Physiology or Medicine in 2005, there have been an increasing number of reports on PubMed as to the relationship between inflammation and carcinogenesis in a variety of tissues (Table 1) and it has been featured in major journals. Table 1: Inflammation and cancer in various tissues. In terms of the large bowel, it has been found that the risk of colorectal cancer increases in relation to the degrees of inflammation and the disease duration (duration/risk = 10 years/1.6%, 20 years/8.3%, and 30 years/18.4%) in inflammatory bowl diseases (IBDs) such as ulcerative colitis (UC) and Crohn¡¯s disease (CD) (Figure 1) [3]. I have been interested in inflammation-associated colorectal carcinogenesis for a long time, since even younger patients with UC have high risk of colorectal cancer [4]. Figure 1: UC patients are high-risk groups of colorectal cancer (CRC) development. Patients with UC as well as those with colorectal cancer have been increasing in Asian countries including Japan, similarly to Western countries (Figure 2) [5]. Therefore, it is necessary to investigate the mechanisms of colorectal cancer development with the background of inflammation for establishing the countermeasure strategy
%U http://www.hindawi.com/journals/iji/2012/658786/