ABSTRACT
Chronic inammation is a recognized risk factor in the development of various cancers. The link between inammation and cancer has been suggested by epidemiological and experimental data (Grivennikov et al. 2010), and conrmed by numerous reports demonstrating that inammatory cells can promote disease by inducing cell proliferation and invasion and supporting cancer cell survival. Chronic inammatory states are now widely accepted as an important factor that leads to an environment fostering genomic lesions, tumor initiation, and progression. For example, epidemiological studies have identied multiple risk factors for colon cancer, with chronic inammation thought to be the leading cause (Rizzo et al. 2011). Meta-analysis has shown that patients suffering from inammatory bowel diseases, such as Crohn’s disease and ulcerative colitis, have a relative risk of developing bowel cancers of 33.2 compared to the general population (Canavan et al. 2006). These diseases affect approximately 1 to 2 of every 1000 people in developed countries and are on the rise worldwide (Molodecky et al. 2012). Links between inammation and cancer have been conrmed in a number of animal models, particularly in the colon (Clapper et al. 2007; Harris et al. 2001), liver (Rogers and Houghton 2009), and pancreas (pancreatitis) (Satake et al. 1986). Chronic inammation is thought to induce DNA modications in the intestinal epithelial cells through the release of reactive oxygen species (ROS) and reactive nitrogen species (RNS) by inammatory cells (Meira et al. 2008; Westbrook et al. 2009) and can result in chromosomal instability as well as DNA methylation (Grady and Carethers 2008).
