ABSTRACT
CONTENTS Epidemiological Correlation of Fiber Intake and Colon Cancer Risk . . . . 296 In Vivo Carcinogenesis Studies in Animal Models . . . . . . . . . . . . . . . . . . . . . . . . . . 297
Inulin-Like Fructans and Reduction of Colon Carcinogenesis in Animal Models . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 297
Resistant Starch and Reduction of Colon Carcinogenesis in Animal Models . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304
Reduction of Colon Carcinogenesis in Animal Models by Further Prebiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305
Reduction of Colon Carcinogenesis in Animal Models by Synbiotics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 306
Mechanisms of Prevention of Colon Carcinogenesis . . . . . . . . . . . . . . . . . 307 Apoptosis and Proliferation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 310 Modulation of Immune Response . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 312 Reduction of Enzyme Activity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 313 Fecal Water Genotoxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 314
In Vitro Studies of Effects of Prebiotics and Their Fermentation Products on Epithelial Colon Cancer Cells . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 314
In Vivo Colon Carcinogenesis Studies in Humans . . . . . . . . . . . . . . . . . . . . . . . . . . . 316 Prebiotics and Anticancer Activities in Other Tumors . . . . . . . . . . . . . . . . . . . . . . 318 Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 319 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 320
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Colon cancer is one of the major neoplastic diseases with the number of new cases per year rising rapidly since 1975. Colon cancer is the fourth commonest form of cancer and causes 12.6% of all cancer incidents in men and 14.1% in women in the westernized countries.1 However, large differences exist between populations worldwide. Epidemiological studies regarding colon cancer risk in communities with different lifestyles and in migrants suggest that 70-80% of colorectal cancers may owe their appearance to “environmental” factors including cultural, social, and lifestyle practices.2 There has been an ongoing debate as to whether an increased intake of dietary fiber is inversely related to decreased colon cancer risk. While a number of prospective studies failed to establish a link between fiber intake and colon cancer incidents,3-5 some recent studies showed an inverse correlation between them. In the EPIC study,6 which followed up 519,978 participants for cancer incidence, participants were categorized into five groups with regard to their consumption of fiber per day. The adjusted relative risk of incidence of large bowel cancer for the highest versus the lowest quintile of fiber from food intake was 0.58 (95%CI: 0.41-0.85) and the protective effect was greatest for the left side colon and least for the rectum. Another study showed that in patients, who had colorectal adenoma removed prior to the study, a low fat, high fiber diet rich in fruit and vegetables lowered the adenoma recurrence in males that did not use nonsteroidal anti-inflammatory drugs.7 Jacobs et al.8
