Abstract

Serrated lesions, as a rule, were considered benign and were likened to hyperplastic polyps by anatomists and gastroenterologists. These views persisted until about 2010. However, recent data showed that serrated lesions can potentially transform into colorectal cancer (CRC). The World Health Organization classification identifies 4 categories of serrated lesions: hyperplastic polyps, sessile serrated lesions, traditional serrated adenoma and unclassified serrated adenomas. Sessile serrated lesions with dysplasia and traditional serrated adenomas are the most common precursors of CRC. Development of CRC from serrated lesions occurs through two different molecular pathways, namely, sporadic microsatellite instability and CpG island methylator phenotype, and the latter is considered the main mechanism inactivating serrated CRC pathway. In contrast to adenoma–carcinoma pathway, APC-inactivating mutations are rare in serrated adenomas.

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