Serrated pathway: alternative route to colorectal cancer

World J Gastroenterol. 2013 Feb 7;19(5):607-15. doi: 10.3748/wjg.v19.i5.607.

Abstract

Serrated polyps have been an area of intense focus for gastroenterologists over the past several years. Contrary to what was thought before, a growing body of literature indicates that these polyps can be precursors of colorectal cancer (CRC). Most of these lesions, particularly those in the proximal colon, have so far been under-recognized and missed during colonoscopy, qualifying these lesions to be the main cause of interval cancers. It is estimated that 10%-20% of CRCs evolve through this alternative, serrated pathway, with a distinct genetic and epigenetic profile. Aberrant DNA methylation plays a central role in the development of this CRC subtype. This characteristic molecular background is reflected in a unique pathological and clinical manifestation different from cancers arising via the traditional pathway. In this review we would like to highlight morphological, molecular and clinical features of this emerging pathway that are essential for gastroenterologists and may influence their everyday practice.

Keywords: Colorectal cancer; DNA methylation; Endoscopic surveillance; Hyperplastic polyps; Serrated adenomas; Serrated pathway.

Publication types

  • Editorial
  • Review

MeSH terms

  • Adenocarcinoma / classification
  • Adenocarcinoma / genetics
  • Adenocarcinoma / metabolism
  • Adenocarcinoma / pathology*
  • Adenocarcinoma / therapy
  • Animals
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / metabolism
  • Cell Transformation, Neoplastic / pathology*
  • Colonic Polyps / classification
  • Colonic Polyps / genetics
  • Colonic Polyps / metabolism
  • Colonic Polyps / pathology*
  • Colonic Polyps / therapy
  • Colorectal Neoplasms / classification
  • Colorectal Neoplasms / genetics
  • Colorectal Neoplasms / metabolism
  • Colorectal Neoplasms / pathology*
  • Colorectal Neoplasms / therapy
  • DNA Methylation
  • Disease Progression
  • Epigenesis, Genetic
  • Gene Expression Regulation, Neoplastic
  • Genetic Predisposition to Disease
  • Humans
  • Hyperplasia
  • Prognosis
  • Signal Transduction