Prevention of colitis-associated cancer: From bench to bed

Abstract

Chronic inflammation is a major risk factor for the development of gastrointestinal cancers, as evidenced with esophageal adenocarcinoma consequent to Barrett’s esophagus, gastric adenocarcinoma after Helicobacter pylori-associated chronic atrophic gastritis, and colon adenocarcinoma relevant to inflammatory bowel disease (IBD). Though not all, these featured carcinogenesis pathway associated chronic inflammation rendered the anticipation of cancer prevention through optimal intervention of antiinflammation. Since the pathogenesis of colitis-associated cancer (CAC) is distinct from sporadic colorectal cancer (CRC), intervening molecular mechanisms underlying CAC featured with inflammatory mutagenic actions, medical therapies that can diminish the mucosal inflammatory response can be chemopreventive strategy, including sulfasalazine, immune modulator, biologics, and some natural phytoceuticals. Furthermore, the elucidation of risk factors implicated in CAC, genetic, pharmacological, and epidemiological aspect based on a large magnitude of data, increased the chance of cancer prevention in this connection between inflammation and carcinogenesis. The altered physiological microenvironment is thought to be responsible for the initiation of CAC, of which the prominent contribution is associated with inflammation, oxidative stress, and proliferation. Therefore, the fundamental treatment modality should incorporate the initial remission, but the overlook of mucosal healing to be from longstanding journey to mutagenesis. In this chapter, we will show the recent advancement in the understanding of CAC as well as possible chance of cancer prevention. © 2017 Nova Science Publishers, Inc.