New cases of colonic cancer were expected to reach 107,000 in 1994 and to cause over 49,000 deaths. The incidence and mortality figures for rectal cancer were 42,000 and 7,000, respectively. The mortality rates for colonic cancer may be somewhat overestimated and those for rectal cancer underestimated because some death certificates state ?colon cancer? when the listed hospital diagnosis was cancer of the rectum or rectosigmoid.
Colorectal cancer increases with age and has increased significantly in white males, black males, and black females between 1973 and 1989. Since 1985, however, there have been declines for white males and females as well as a small decline for black females. Moreover, mortality rates have declined for white males and females and for black females but increased for black males in the 1985 to 1989 reporting period. This is most likely due to earlier diagnosis, since more than one-third of colorectal cancer patients are now diagnosed while the cancer is still localized. Five-year survival rates are about 90% when the cancer is detected while still localized; they fall of rapidly with spread of the disease. Survival rates for patients with distant metastases are less than 7%.
A number of predisposing factors have been identified for colorectal cancer. These include familial adenomatous polyposis, chronic ulcerative colitis, and the ?cancer family syndrome.? There is also a correlation with high-fat, low-fiber diets, although the cause-effect relationship between diet and colorectal cancer is not clearly understood.
Familial polyposis is all inherited autosomal dominant trait that leads to the production of multiple adenomatous polyps in the colon. These polyps have a tendency to undergo malignant transformation by age 30. In familial polyposis, all associated gene mutation has been identified. In one study, mutations of the affected gene, called APC, were found in the earliest tumors that were analyzed, including adenomas 0.5 cm in diameter, and the frequency of mutations remained constant as benign adenomas progressed to adenocarcinomas. These data indicate that mutations of the APC gene, thought to he a tumor suppressor gene, play a major role in initiation of colonic cancer. Other genetic changes such as mutations to the ras oncogene and in the p53 tumor suppressor gene occur later in tumor progression than alteration of the APC gene.
Treatment of colonic cancer may he by surgery, radiation therapy, chemotherapy, or a combination of treatment modalities, depending on the stage and location of the tumor. Surgery with or without radiation therapy is the most effective treatment, but survival is closely correlated with early detection of localized disease. Chemotherapy by itself is minimally effective in this disease, but combinations of 5-f1uorouracil (5-FU) and immune system stimulators such as levamisole or 5-FU plus leucovorin have shown some promise. The mechanism of action and side effects of leucovorin are high-yield subjects you should know for USMLE Step 1.
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