Abstract
Sporadic colon cancers develop as a result of a sequence of genetic events that cause mutation or deletion of key regulator genes, resulting first in hyperplasia, then adenoma, and subsequently, carcinoma and metastasis. This can occur as a result of mutations causing a loss of heterozygosity in key genes such as FAP, DCC, K-ras, and p53 themselves, or as a result from damage to the mismatch repair genes that allow the cell to repair errors in DNA. Genes with a role in colon carcinogenesis include more recently understood genes such as matrix-metalloproteinases, Bcl-2, and VEGF, some of which may provide potential prognostic information and targets for novel therapies.
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