Colon cancer is the third and second most common cancer form in men and women worldwide, causing appropriate 640 thousand deaths each year. It is generally accepted that colon cancer mainly results from diet cancer mainly results from diet.Colon cancer is believed the result of a cascade of genetic mutations leading to progressively disordered local DNA replication and accelerated colonocyte mitosis. Progressive accumulation of multiple genetic mutations results in the transition from normal mucosa to benign adenoma to severe dysplasia to frank carcinoma. Malfunction of the mismatch repair genes may account for approximately 15% of sporadic colon cancers. In the HNPCC syndrome, the mismatch repair genes malfunction because of genetic mutation.In sporadic serrated adenomas, the mismatch repair gene hMLH1 often malfunctions because of DNA hypermethylation. APC mutation is believed to account for approximately 80% to 85% of sporadic colon cancers. Colon cancer may arise in inflammatory bowel disease from a different but so far uncharacterized pathway.
The k-ras gene encodes for a protein involved in signal transduction from the cell membrane to the nucleus. Specific mutations of this gene activate this signal pathway and promote colonocyte replication. These mutations are associated with exophytic growth of adenomas in the transition to carcinoma. Approximately 50% of colon cancers have k-ras mutations. Mutation of the p53 gene is believed important in the transition from advanced adenoma to frank carcinoma. Approximately 50% of colonic lesions with high-grade dysplasia and approximately 75% of frank cancers exhibit p53 mutations

References

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