Summary
Several lines of evidence suggest that bile acids may be implicated in the pathogenesis of colonic cancer. A high consumption of fat and animal protein and a low dietary intake of fiber have been shown to be related to the incidence of colonic cancer. From these epidemiologic observations the hypothesis was proposed that the correlation between diet and colon cancer might be explained by the involvement of bile acids. Populations at a high risk of developing cancer were shown to have an increased excretion both of total and bacterially modified bile acids in their feces. Animal studies demonstrated a cocarcinogenic effect of bile acids and experimental diets containing large amounts of fat did not only induce an increased bile acid excretion but also an enhanced tumor formation in the colon. Furthermore, microbial in vitro tests showed a comutagenic activity of secondary bile acids. However, case control studies comparing the fecal bile acid excretion pattern in colonic cancer patients and control subjects failed to show such a clear relationship, which might be explained by rather similar dietary habits within one population and individual differences in sensitivity to environmental factors contributing to the tumor development. Cholecystectomy, leading to an increased exposure of bile acids to the intestinal microflora, has been suggested as a predisposing factor for the development of colonic cancer, but the results of experimental and epidemiologic studies so far are rather inconsistent. More recent studies of epithelial cell kinetics showed that bile acids alter cell proliferative activity in the colonic mucosa by increasing the number of DNA synthesizing cells and expanding the proliferative compartment up to the middle third of the crypt. This enhanced cell proliferation seems to be related to the bile acid induced tumor formation due to an increased opportunity of malignant transformation. Bile acids may be implicated in the causation of human colonic cancer by stimulating the growth of a small-size benign adenoma to a large size with a correspondingly high risk of malignancy.
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Breuer, N., Goebell, H. The role of bile acids in colonic carcinogenesis. Klin Wochenschr 63, 97–105 (1985). https://doi.org/10.1007/BF01734247
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DOI: https://doi.org/10.1007/BF01734247

