Advances in molecular biology have defined the molecular basis for colorectal cancer (CRC). Although only a fraction of CRC has been determined to have a hereditary component, the discovery of genetic alterations in these clinical syndromes has permitted definition of similar discoveries in sporadic CRC. Here we delineate the molecular basis for the most common of these defined syndromes, including familial adenomatous polyposis, hereditary nonpolyposis colon cancer, MUTYH-associated polyposis, juvenile polyposis, Peutz-Jeghers syndrome, and Cowden's syndrome. The newest paradigm with implications for the pathogenesis of sporadic CRC is called the cancer stem cell hypothesis. As this paradigm also implicates aberrations in molecular pathways, a brief discussion of this hypothesis is included.
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