Cancer of the colon and rectum (colorectal cancer) affects nearly 160,000 Americans each year, causing approximately 62,070 deaths annually. Colorectal cancer ranks fourth worldwide in cancer occurrence and deaths (Shibuya K et al 2002), though it has a better prognosis than do most cancers. In the general population, the risk of developing colorectal cancer is approximately 19 percent, and it is estimated that 2 percent to 5 percent of sporadic polyps will develop into an invasive cancer (Markowitz AJ et al 1997). Therefore, early detection of colorectal cancer dramatically increases survival (Weir HK et al 2003). For example, 90 percent of patients who receive treatment before the cancer has spread are alive after five years, compared to only 10 percent who survive if the cancer is widespread and treated conventionally (Dashwood RH 1999).

The lifetime risk of developing colorectal cancer is 4.6 percent for men and 3.2 percent for women (Chu KC et al 1994). Its occurrence is higher in developed countries and in African-Americans versus Caucasians. The peak age of onset of colorectal cancer in the United States is 65 (Khan A et al 2002).

Together, the colon and rectum make up the large intestine, which is located in the abdomen and pelvis, and the term “colorectal cancer” refers to cancers of both areas. The function of the colon is storage, concentration, and propulsion of undigested material toward the rectum and anus for the purpose of defecation (i.e., a bowel movement).

A colorectal carcinoma is a malignant (cancerous) new growth that arises from cells in the bowel lining. Carcinomas tend to invade nearby tissue and spread (metastasize) to distant organs such as the liver, lungs, bone, and brain. Adenocarcinoma of the colon and rectum develops in the glands of the intestine’s inner lining (mucosa) and accounts for 95 percent of colorectal cancer cases.

Colorectal cancer develops through a process involving genetic change in the epithelial cells of the colon lining. The main factors that initiate colorectal cancer are consumption of cooked red meat (due to heterocyclic amines) (Gerhardsson de V et al 1991; Reddy S et al 1987), high intake of refined carbohydrates (Franceschi S et al 2001), poor vitamin and mineral intake, alcohol consumption, smoking, bile acids, fecal mutagens (DNA-damaging agents), fecal pH, and compromised detoxification enzymes (Winawer SJ et al 1992). An example of one important detoxification enzyme is N-acetyltransferase, which catalyzes the formation of DNA-damaging products from heterocyclic amines that form in cooked meats. Differences in the activity of this enzyme classify individuals as slow or fast acetylators. The level of red meat consumption in fast but not slow acetylators is associated with risk for colorectal cancer development (Welfare MR et al 1997).

Individuals at high risk of developing colorectal cancer can be identified by their age (older than 40), genetic factors such as familial polyposis syndromes, hereditary nonpolyposis colon cancer (Boutron MC et al 1995; Grossman S et al 1988), or a personal or family history of colon carcinoma or polyps (Collett JA et al 1999; Foutch PG et al 1991). Other predisposing conditions include inflammatory bowel disease (particularly ulcerative colitis), Crohn’s disease (Karlen P et al 1999), pelvic irradiation (Neugut AI et al 1991), high fasting glucose level, high insulin level, and diabetes mellitus (Ma J et al 1999; Schoen RE et al 1999). Other risk factors include poor diet (Evans RC et al 2002; Martinez ME et al 1999; Russo A et al 1998), lifestyle, lack of exercise (Giovannucci E et al 1996a), tobacco (Lieberman DA et al 2003; Giovannucci E et al 1996b) and alcohol use (Nagata C et al 1999; Giovannucci E et al 1998, 2003), overeating, and nonsteroidal anti-inflammatory drug (NSAID) use.