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Pathology Research International
Volume 2011 (2011), Article ID 157073, 13 pages
http://dx.doi.org/10.4061/2011/157073
Review Article

Serrated Polyposis: An Enigmatic Model of Colorectal Cancer Predisposition

1Pathology Queensland and UQ Centre for Clinical Research, Royal Brisbane and Women’s Hospital, Herston, QLD 4029, Australia
2Familial Cancer Laboratory, QIMR, 300 Herston Road, Herston, QLD 4006, Australia
3New Zealand Familial Gastrointestinal Cancer Registry, Auckland City Hospital, Auckland 1142, New Zealand
4Department of Gastroenterology and Hepatology, Middlemore Hospital, Auckland 1640, New Zealand
5The University of Queensland School of Medicine, Herston, QLD 4006, Australia

Received 11 November 2010; Revised 12 February 2011; Accepted 25 February 2011

Academic Editor: Wade Samowitz

Copyright © 2011 Christophe Rosty et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Serrated polyposis has only recently been accepted as a condition which carries an increased personal and familial risk of colorectal cancer. Described over four decades ago, it remains one of the most underrecognized and poorly understood of all the intestinal polyposes. With a variety of phenotypic presentations, it is likely that serrated polyposis represents a group of diseases rather than a single entity. Further, neoplastic progression in serrated polyposis may be associated with premature aging in the normal mucosa, typified by widespread gene promoter hypermethylation. From this epigenetically altered field, arise diverse polyps and cancers which show a range of molecular features. Despite a high serrated polyp count, only one-third of colorectal cancers demonstrate a BRAF V600E mutation, the molecular hallmark of the canonical serrated pathway, suggesting that though multiple serrated polyps act as a marker of an abnormal mucosa, the majority of CRC in these patients arise within lesions other than BRAF-mutated serrated polyps.