Colon cancer is the second most common cause of cancer mortality among adults in the United States today (1 ). Colon cancer arises from a pathological transformation of the normal colonic epithelium to an adenomatous polyp, which can then progress to an invasive tumor. This progression is brought about by a number of genetic changes, which include the inactivation of tumor suppressor genes and activation of protooncogenes, the net result of which is to confer a proliferative advantage to the cancerous cell (2 ,3 ). These changes are best described in the colon cancer adenoma-carcinoma sequence model as outlined in Fig. 1 (4 ).
