Colorectal Cancer

One of the earliest examples of surgical prophylaxis is the recommendation for total proctocolectomy for subsets of patients with chronic ulcerative colitis. Patients with pancolitis, onset of disease at a young age, and a long duration of colitis are at high risk of developing colorectal cancer.36 Other clinical diseases of the large intestine also illustrate the role of proctocolectomy in cancer prevention. Familial adenomatous polyposis coli (FAP) syndrome, defined by the diffuse involvement of the colon and rectum with adenomatous polyps often in the second or third decade of life, almost always predisposes to colorectal cancer if the large intestine is left in place. However, the role of screening and prophylactic proctocolectomy changed dramatically with the identification of the gene responsible for FAP, the adenomatous polyposis coli (APC) gene, located on the long arm of chromosome 5 (5q21).37 Now, children of families in which an APC mutation has been identified can have genetic testing before polyps become evident. Carriers can have screening and surgical resection once polyps appear, usually in the late teens or early twenties. Although not ideal, the palatability of proctocolectomy in this population was furthered with the description of the total abdominal colectomy, mucosal proc-tectomy, and ileoanal pouch anastomosis.38

As we identify additional syndromes and genes that carry an increased risk of colorectal cancer, the potential role of screening and prophylactic surgery also expands. Hereditary nonpolyposis colorectal carcinoma (HNPCC), or Lynch syndrome, is an autosomal dominant disorder that is estimated to be responsible for 5% to 10% of all colorectal cancers. Although the carcinomas arise from benign adenomas, HNPCC is not characterized by a large number of polyps. Two Lynch syndromes have been described. Lynch syndrome I features an early age onset of cancer, often metachronous. Lynch syndrome II involves cancers not only of the small and large intestine but also endometrial, ovarian, renal, gastric, and hepatobiliary. Although the genes responsible for HNPCC

have been identified, namely hMSHl, hMLHl, hPMSl, and hPMS2, these mutations do not have a 100% penetrance; thus, cancer will not develop in all carriers. Prophylactic surgery is recommended for some but not all carriers, but aggressive screening should be implemented and a subtotal colectomy should be performed if a cancer develops.39,40

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