Published online Sep 14, 2016. doi: 10.3748/wjg.v22.i34.7754
Peer-review started: May 8, 2016
First decision: June 20, 2016
Revised: July 9, 2016
Accepted: July 31, 2016
Article in press: August 1, 2016
Published online: September 14, 2016
It is currently known that colorectal cancers (CRC) arise from 3 different pathways: the adenoma to carcinoma chromosomal instability pathway (50%-70%); the mutator “Lynch syndrome” route (3%-5%); and the serrated pathway (30%-35%). The World Health Organization has classified serrated polyps into three types of lesions: hyperplastic polyps (HP), sessile serrated adenomas/polyps (SSA/P) and traditional serrated adenomas (TSA), the latter two strongly associated with development of CRCs. HPs do not cause cancer and TSAs are rare. SSA/P appear to be the responsible precursor lesion for the development of cancers through the serrated pathway. Both HPs and SSA/Ps appear morphologically similar. SSA/P are difficult to detect. The margins are normally inconspicuous. En bloc resection of these polyps can hence be troublesome. A careful examination of borders, submucosal injection of a dye solution (for larger lesions) and resection of a rim of normal tissue around the lesion may ensure total eradication of these lesions.
Core tip: Colorectal cancers (CRC) arise from 3 pathways: adenoma to carcinoma; “Lynch syndrome”; and serrated. There are 3 types of serrated lesions namely: Hyperplastic Polyps, Sessile Serrated Adenomas/Polyps and Traditional Serrated Adenomas, the latter two are associated with CRC. A careful examination of borders, submucosal injection with dye and ensuring that a rim of normal tissue is removed is paramount.