Human pathology
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Adenocarcinoma of the large intestine can no longer be considered one disease but rather a family of diseases with different precursor lesions, different molecular pathways, and different end-stage carcinomas with varying prognoses. Approximately 60% of colorectal carcinomas arise from conventional adenomas via the suppressor pathway leading to microsatellite stable carcinomas. These carcinomas represent the pathway that has been the target of screening and prevention programs to date. ⋯ Carcinomas arising from sessile serrated adenomas/polyps are not prevented by removing conventional adenomas and hence may be missed in routine screening programs. In addition, a subset of these lesions may potentially progress rapidly to carcinoma; hence, it is likely that these lesions will require a different screening strategy from that used for conventional adenomas. This article reviews the various pathways to colorectal carcinoma with emphasis on the serrated pathway and evaluates the implications of this pathway for colorectal carcinomas screening programs.