Sessile serrated adenoma/polyps: Where are we at in 2016?

Sessile serrated adenoma/polyps: Where are we at in 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 t...

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Main Authors: Singh, Rajvinder, Zorrón Cheng Tao Pu, Leonardo, Koay, Doreen, Burt, Alastair
Format: Online
Language:English
Published: Baishideng Publishing Group Inc 2016
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5016375/
id pubmed-5016375
recordtype oai_dc
spelling pubmed-50163752016-09-27 Sessile serrated adenoma/polyps: Where are we at in 2016? Singh, Rajvinder Zorrón Cheng Tao Pu, Leonardo Koay, Doreen Burt, Alastair Minireviews 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. Baishideng Publishing Group Inc 2016-09-14 2016-09-14 /pmc/articles/PMC5016375/ /pubmed/27678358 http://dx.doi.org/10.3748/wjg.v22.i34.7754 Text en ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Singh, Rajvinder
Zorrón Cheng Tao Pu, Leonardo
Koay, Doreen
Burt, Alastair
spellingShingle Singh, Rajvinder
Zorrón Cheng Tao Pu, Leonardo
Koay, Doreen
Burt, Alastair
Sessile serrated adenoma/polyps: Where are we at in 2016?
author_facet Singh, Rajvinder
Zorrón Cheng Tao Pu, Leonardo
Koay, Doreen
Burt, Alastair
author_sort Singh, Rajvinder
title Sessile serrated adenoma/polyps: Where are we at in 2016?
title_short Sessile serrated adenoma/polyps: Where are we at in 2016?
title_full Sessile serrated adenoma/polyps: Where are we at in 2016?
title_fullStr Sessile serrated adenoma/polyps: Where are we at in 2016?
title_full_unstemmed Sessile serrated adenoma/polyps: Where are we at in 2016?
title_sort sessile serrated adenoma/polyps: where are we at in 2016?
description 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.
publisher Baishideng Publishing Group Inc
publishDate 2016
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5016375/
_version_ 1613646737650483200

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