Carcinogenesis is a multistep process, which can arise from a
combination of mutations in oncogenes or tumor suppressor
genes or from epigenetic changes in DNA such as methylation.
A genetic model describing the transition from healthy colonic
epithelia through increasingly dysplastic adenoma to malignant
cancer has been proposed (5) that identifies a number of key
oncogenes and tumor suppressor genes, the progressive acquisition
of activating or loss of function mutations in which drives
the adenoma to carcinoma transition (Fig. 1). Certain of the
genes identified in this pathway, including adenomatous polyposis
coli (APC) and the DNA mismatch repair (MMR) genes,
are the same as those mutated in familial colorectal cancer
syndromes (