ABSTRACT
Inammation is an adaptive host defense against infection and injury and is primarily a self-limiting process; however, inadequate resolution of inammation could often lead to different chronic diseases, including cancer (Ullman et al. 2011; Kundu and Surh 2008; Schottenfeld and Beebe-Dimmer 2006; Jackson and Evers 2006). It has been estimated that approximately 25% of human cancers are associated with chronic infection and inammation (Hussain and Harris 2007). For example, the development of stomach cancer is strongly associated with Helicobacter pylori-induced gastric inammation (Peek and Blaser 2002). The development of liver cancer is strongly associated with hepatitis B or hepatitis C virus-induced chronic hepatic inammation (Matsuzaki et al. 2007). The development of esophageal adenocarcinoma (EAC) is strongly associated with gastroesophageal reux inammation of the esophagus (Kruse et al. 1993; Altorki et al. 1997). Inammatory bowel disorders such as ulcerative colitis (UC) and Crohn’s disease predispose individuals to the development of colorectal cancer (Ullman et al. 2011; Seril et al. 2003). Several lines of evidence from
3.1 Introduction ............................................................................................................................ 41 3.2 Human EAC ............................................................................................................................ 42 3.3 Animal Models for EAC ......................................................................................................... 43 3.4 Mechanistic Considerations and Prevention of EAC Formation ............................................ 45 3.5 UC-Associated Colorectal Cancer in Humans ....................................................................... 47 3.6 Animal Models for UC-Associated Colorectal Cancer .......................................................... 47 3.7 Mechanistic Consideration and Prevention Studies of UC-Associated Colorectal
Carcinogenesis ........................................................................................................................ 49 3.8 Concluding Remarks on Inammation-Induced Esophageal and Colorectal
Adenocarcinomas ...................................................................................................................50 Acknowledgments ............................................................................................................................50 References ........................................................................................................................................50
