Inflamm Bowel Dis
March 2023
Background And Purpose: Interest in the possibility that diet might help to reduce the risk of colorectal cancer dates back to 1970 based on both the large variation in rates of specific cancers in different countries and the impressive changes observed in the incidence of cancer in migrants from low- to high-risk areas. Here, we report the state of art of literature data about this topic.
Methods: Three sections have been separately considered: chemoprevention of first tumor onset, chemoprevention of recurrence after surgery, and chemoprevention of polyp recurrence in the course of the follow-up of subjects with elevated risk.
Introduction: Colorectal cancer is the third cause of death in industrialized countries. Genetic susceptibility and diet are determinant of cancer risk and tumor behavior. Variation in cancer incidence among and within populations with similar dietary patterns suggests that an individual response may reflect interactions with genetic factors, which may modify gene, protein, and metabolite expression patterns.
View Article and Find Full Text PDFMost sporadic colorectal cancers (CRCs) develop through the adenoma-carcinoma sequence pathway and are initiated by adenomatous polyposis coli (APC) gene mutations. Estrogen receptor beta (ERbeta) is recognized to progressively reduce its expression in adenomatous and carcinomatous tissues in humans. Moreover, ERbeta deficiency enhances small intestinal tumorigenesis in rodents.
View Article and Find Full Text PDFEpidemiological and experimental studies suggest a protective role of estrogens against colorectal cancer. This effect seems to be mediated by their binding to estrogen receptor beta (ER-beta), one of the two estrogen receptors with high affinity for these hormones. Very recently, the demonstration of an involvement of ER-beta in the development of adenomatous polyps of the colon has also been documented, suggesting the use of selective ER-beta agonists in primary colorectal cancer prevention.
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