Fig. 6.02 Male incidence (blue) and mortality (orange) of colorectal cancer in some selected countries.

From: Globocan, IARC Press, Lyon.

Fig. 6.01 Worldwide annual incidence (per 100,000) of colon and rectum cancer in males. Numbers on the map indicate regional average values. From: Globocan, IARC Press, Lyon.

Fig. 6.02 Male incidence (blue) and mortality (orange) of colorectal cancer in some selected countries.

From: Globocan, IARC Press, Lyon.

with a sedentary lifestyle. Epidemiological studies have indicate that meat consumption, smoking and alcohol consumption are risk factors. Inverse associations include vegetable consumption, prolonged use of non-steroidal anti-inflammatory drugs, oestrogen replacement therapy, and physical activity {1531, 2121}. Fibre may have a protective role, but this has been questioned recently. The molecular pathways underlying these epidemiological associations are poorly understood, but production of het-erocyclic amines during cooking of meat, stimulation of higher levels of fecal bile acids and production of reactive oxygen species have been implicated as possible mechanisms {416, 1439}. Vegetable anticarcinogens such as folate, antioxidants and inducers of detoxifying enzymes, binding of luminal carcinogens, fibre fermentation to produce protective volatile fatty acids, and reduced contact time with colorectal epithelium due to faster transit may explain some of the inverse associations.

Chronic inflammation

Chronic inflammatory bowel diseases are significant aetiological factors in the development of colorectal adenocarcinomas {1582}. The risk increases after 8-10 years and is highest in patients with early-onset and widespread manifestation (pancolitis).

Ulcerative colitis. This chronic disorder of unknown aetiology affects children and adults, with a peak incidence in the early third decade. It is considered a pre-malignant disorder, with duration and extent of disease being the major risk factors. Population-based studies show a 4.4-fold increase in mortality from col-

Fig. 6.04 A Depressed lesion highlighted with indigo-carmine dye spray corresponding to high-grade intraepithelial neoplasia. B Flat, elevated adenoma with high-grade intraepithelial neoplasia after indigo-carmine dye spray.

orectal carcinoma {1504, 448, 1835, 1214}. In clinical studies, the increase in incidence is usually higher, up to 20-fold {647, 990}. Involvement of greater than one half of the colon is associated with a risk to develop carcinoma of approximately 15%, whereas left sided disease may bear a malignancy risk of 5% {1727, 1045}. Ulcerative proctitis is not associated with an increased carcinoma risk. Crohn disease. Development of carcinoma is seen both in the small intestine and the large intestine. The risk of colorectal malignancy appears to be 3 fold above normal {581}. Long duration and early onset of disease are risk factors for carcinoma.

Modifying factors. Non-steroidal anti-inflammatory drugs and some naturally occurring compounds block the biochemical abnormalities in prostaglandin homeostasis in colorectal neoplasms. Some of these agents cause a dramatic involution of adenomas but their role in the chemoprevention of adenocarcinoma is less clear. Polymorphisms in key enzymes can alter other metabolic pathways that modify protective or injurious compounds, e.g. methylenetetrahydrofo-late reductase, N-acetyltransferases, glu-tathione-S-transferases, aldehyde dehy-drogenase and cytochrome P-450 {1766, 686, 1300}. These polymorphisms may explain individual susceptibility or predisposition among populations with similar exposures {1555}.


A rare but well recognized aetiological factor in colorectal neoplasia is therapeutic pelvic irradiation {1974}.

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