In this article, the incidence, mortality, and survival rates for colorectal cancer are reviewed, with attention paid to regional variations and changes over time. A concise overview of known risk factors associated with colorectal cancer is provided, including familial and hereditary factors, as well as environmental lifestyle-related risk factors such as physical inactivity, obesity, smoking, and alcohol consumption.KEYWORDS: Colorectal cancer, epidemiology, incidence, survival, risk factorsObjectives: Upon completion of this article, the reader should be able to identify epidemiologic trends in the incidence, mortality, and survival rates for colorectal cancer across different patient demographics; describe familial and hereditary risk factors associated with the development of colorectal cancer; and list dietary and lifestyle factors known to be associated with the risk of colorectal cancer. INCIDENCE OF COLORECTAL CANCERColorectal cancer is a major cause of morbidity and mortality throughout the world.1 It accounts for over 9% of all cancer incidence. 2,3 It is the third most common cancer worldwide and the fourth most common cause of death.2 It affects men and women almost equally, with just over 1 million new cases recorded in 2002, the most recent year for which international estimates are available.

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Glucagon-like peptides (GLPs) are secreted from enteroendocrine cells in the gastrointestinal tract. GLP-1 actions regulate blood glucose, whereas GLP-2 exerts trophic effects on intestinal mucosal epithelium. Although GLP-1 actions are preserved in diseases such as diabetes, GLP-2 action has not been extensively studied in the setting of intestinal disease. We have now evaluated the biological effects of a human GLP-2 analog in the setting of experimental murine nonsteroidal antiinflammatory drug-induced enteritis. Human (h)[Gly2]GLP-2 significantly improved survival whether administered before, concomitant with, or after indomethacin. h[Gly2]GLP-2-treated mice exhibited reduced histological evidence of disease activity, fewer intestinal ulcerations, and decreased myeloperoxidase activity in the small bowel ( P < 0.05, h[Gly2]GLP-2- vs. saline-treated controls). h[Gly2]GLP-2 significantly reduced cytokine induction, bacteremia, and the percentage of positive splenic and hepatic bacterial cultures ( P < 0.05). h[Gly2]GLP-2 enhanced epithelial proliferation ( P < 0.05 for increased crypt cell proliferation in h[Gly2]GLP-2- vs. saline-treated mice after indomethacin) and reduced apoptosis in the crypt compartment ( P < 0.02). These observations demonstrate that a human GLP-2 analog exerts multiple complementary actions that serve to preserve the integrity of the mucosal epithelium in experimental gastrointestinal injury in vivo.