Abstract
Research in the causes of colorectal cancer (CRC) has accelerated at an explosive rate during the past two decades. 1 Much has changed since Sklifasowski 2 first noted the connection between polyps and CRC. Its genetic implications subsequently led to the characterization of familial adenomatous polyposis (FAP), which is unquestionably the best known example of hereditary (autosomal-dominant) CRC. Familial adenomatous polyposis has been a great teacher. It had been considered for many decades to be a very simplistic disease, with its phenotype (colonic polyps and cancer) restricted to the colon. However, in the early 1950s, Gardner and Richards 3 significantly changed this concept when they described extracolonic signs, namely, cutaneous (epidermoid cysts) and osseous (osteomas), in a large kindred prone to colonic polyps and CRC. This variant is now known as Gardner's syndrome. Nakamura et al 4 subsequently showed that Gardner's syndrome was linked to the FAP locus on the
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