Abstract
Colorectal cancers develop, mature, and metastasize when a compendium of genetic and epigenetic lesions in a colonic stem cell accumulate to cause dysregulation of a variety of cellular processes, including multiple growth regulatory signaling pathways.1 Genomic instability seems to drive the process of formation of colorectal cancers from normal colonic epithelium to adenoma to carcinoma, and perhaps through metastasis. This genomic instability—either chromosomal instability, microsatellite instability, or forms of epigenetic instability—may seem to damage the genome randomly, but ultimately accrues a nonrandom aggregation of very specific targets that are deregulated and allow the establishment of an initial colorectal neoplasm, or further drive an early neoplasm to malignant transformation and eventual distal spread.1
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