Colon Cancer

Cancer is one of the main causes of mortality in the industrialized world, yet the incidence of colon cancer varies worldwide. Bowel cancer is the second most common cancer in the UK, after breast cancer in women and lung cancer in men. Far Eastern populations, such as China and Japan, used to have a much lower incidence [132].Up to the 1960s, prostate cancer was rare in Japan and Far East countries. The apparent protection of an Asian heritage is speculated to probably be dietary which can be lost upon adoption of a Western style diet [118,133]. Soy is a particular component of Far Eastern diets, not present in the traditional Western diet. There have been several case-control studies examining a role for soybean in protection against colo-rectal cancer, in China, Japan and in Japanese migrants to the US [64]. However, there is not a clear relationship because studies have yielded non-significant results.

Many hypotheses have suggested lignans to be the active chemoprotective agent, but there has been little investigation of lignan intake or excretion in relation to bowel cancer [134,135]. Many speculations which have suggested lignans' role in the protection against colon cancer have been extrapolated from the beneficial effects of a well-balanced diet, which is high in dietary fiber. Slattery et al. [136] evaluated the diet diversity, diet composition and risk of colon cancer in an incident population-based study of 1,993 cases and 2,410 controls. Total diet diversity was not associated with colon cancer. However, eating a diet with greater diversity of meats, poultry, fish and eggs, was associated with a 50% increase in risk among all men with a slightly stronger association for younger men and men with distal tumors. A diet with a greater number of refined grain products was also associated with increased risk among men. Women who ate a diet with a more diverse pattern of vegetables were approximately at a 20% lower risk than women who had the least diverse diet in vegetables. In addition, a high intake of dietary fiber has been thought to reduce the risk of colorectal cancer and adenoma [137]. However, in a recent large prospective study with a follow-up extending to 16 years, Fuchs et al. [138] found no association between the intake of dietary fiber and the risk of col-orectal cancer.

Colon cancer does not have a strong association with hormone status, but there are a number of other possible mechanisms whereby lignans or iso-flavones could be involved in the etiology of bowel cancer. For example, there may be a role for isoflavones to inhibit endogenous N-nitrosation that occurs when meat is consumed via suppression of inducible NO synthase [139]. In animals, aberrant crypts are accepted early markers of colon cancer which can be induced by standard chemical carcinogens. One study has shown that linseed is able to reduce the numbers of these aberrant crypts formed in such animal models, and another study has shown that genistein has the same effect [140, 141]. Genistein was found to inhibit azoxymethane (AOM)-induced formation of aberrant crypts in the colon of male F344 rats [142]. These studies provided a rationale for the evaluation of genistein in the long-term pre-clinical colonic tumor assay for a closer assessment of the potential utility of this agent. In addition, Sung et al. [143] determined that, at 100 |M concentrations, lignans significantly reduced the proliferation of colon tumor cells. The growth was not affected by the presence of E2, implying that these cells are not estrogen-sensitive. Although evidence for the presence of ER in the colon in inconsistent [144], tamoxifen, a synthetic anti-estrogen, has demonstrated growth inhibitory effects on colon tumor cells [145]. In contrast, Rao et al. [146] demonstrated that the administration of genistein significantly increased non-invasive and total adeno-carcinoma multiplicity in the colon, compared to the control diet, but had no effect on the colon adenocarcinoma incidence or on the multiplicity of invasive adenocarcinoma. The results of this investigation emphasize that the biological effects of genistein may be organ specific, inhibiting cancer development in some sites yet showing no effect or enhancing effects on the tumorigenesis at other sites, such as the colon. The exact mechanism(s) of colon tumor enhancement by genistein remains to be elucidated. The data regarding dietary estrogens and colon cancer are still limited and need to be investigated further.

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