Serrated polyps and colorectal cancer risk

Abstract

SUMMARY Colorectal cancer is among the three most common cancers in the World with a global incidence exceeding 1.2 million new cases and 600,000 deaths per year; yet most cases could be prevented by endoscopic removal of precursor lesions. Efficient screening and follow-up are the best options to reduce the cancer burden caused by colorectal cancer (CRC). Therefore, it is essential to know which colorectal polyps have the potential to progress into cancer. During the last decade, serrated polyps have emerged as the second most important group of CRC precursor lesions, in addition to conventional adenomatous polyps. It has been estimated that up to 30–35% of CRCs have their origin in serrated polyps. Carcinogenesis via serrated polyps, known as the serrated pathway, requires activation of the MAPK pathway by mutations of BRAF and KRAS, and low- or high-level methylation of CpG islands of DNA (CpG island methylator phenotype), and subsequent high-level DNA microsatellite instability in a third of cases. The mechanisms involved in carcinogenesis via the serrated pathway profoundly differ from those of conventional adenoma–carcinoma pathway, and the biology and behavior of serrated polyps also differ from that of adenomatous polyps, which are characterized by chromosomal instability and loss of tumor suppressor genes.

Financial & competing interests disclosure

This work has been supported by the Academy of Finland, Emil Aaltonen Foundation and Finnish Cancer Foundation. The author has no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Notes

HP: Hyperplastic polyp.

Data taken from [9].

Data taken from [9].

Additional information

Funding

This work has been supported by the Academy of Finland, Emil Aaltonen Foundation and Finnish Cancer Foundation. The author has no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.