gamma-sitosterol and Intestinal-Polyps

Adenoma formation in the colon has been shown to be initiated by an alteration in the genetic make-up which controls the repopulation of the mucosa. This defect is recognized primarily by an upward displacement of the major zone of DNA synthesis within one or a few crypts. Progression to a microadenoma involves an elevation of cell proliferation within these glands and may be hastened by mucosal responses to environmental and dietary factors which enhance cell turnover. The high proliferative activity of epithelial cells within these select crypts allows the unmasking of the neoplastic genotype and the expansion of these cells with a proliferative advantage. Continued rapid cell proliferation within the adenoma either indigenous to the excrescence or fueled additionally by luminal conditions may contribute to the evolution of a malignant genotype, the establishment of a severely dysplastic clone and ultimately to the production of invasive colon cancer.

Topics: Adult; Animals; Antioxidants; Colon; Colonic Neoplasms; Humans; Intestinal Polyps; Mice; Middle Aged; Neoplasms, Experimental; Precancerous Conditions; Rats; Sitosterols