Serrated Colorectal Lesions: An Up-to-Date Review from Histological Pattern to Molecular Pathogenesis

Until 2010, colorectal serrated lesions were generally considered as harmless lesions and reported as hyperplastic polyps (HPs) by pathologists and gastroenterologists. However, recent evidence showed that they may bear the potential to develop into colorectal carcinoma (CRC). Therefore, the World H...

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Main Authors: Martino Mezzapesa, Giuseppe Losurdo, Francesca Celiberto, Salvatore Rizzi, Antonio d’Amati, Domenico Piscitelli, Enzo Ierardi, Alfredo Di Leo
Format: Article
Language:English
Published: MDPI AG 2022-04-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/23/8/4461
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author Martino Mezzapesa
Giuseppe Losurdo
Francesca Celiberto
Salvatore Rizzi
Antonio d’Amati
Domenico Piscitelli
Enzo Ierardi
Alfredo Di Leo
author_facet Martino Mezzapesa
Giuseppe Losurdo
Francesca Celiberto
Salvatore Rizzi
Antonio d’Amati
Domenico Piscitelli
Enzo Ierardi
Alfredo Di Leo
author_sort Martino Mezzapesa
collection DOAJ
description Until 2010, colorectal serrated lesions were generally considered as harmless lesions and reported as hyperplastic polyps (HPs) by pathologists and gastroenterologists. However, recent evidence showed that they may bear the potential to develop into colorectal carcinoma (CRC). Therefore, the World Health Organization (WHO) classification has identified four categories of serrated lesions: hyperplastic polyps (HPs), sessile serrated lesions (SSLs), traditional serrated adenoma (TSAs) and unclassified serrated adenomas. SSLs with dysplasia and TSAs are the most common precursors of CRC. CRCs arising from serrated lesions originate via two different molecular pathways, namely sporadic microsatellite instability (MSI) and the CpG island methylator phenotype (CIMP), the latter being considered as the major mechanism that drives the serrated pathway towards CRC. Unlike CRCs arising through the adenoma–carcinoma pathway, APC-inactivating mutations are rarely shown in the serrated neoplasia pathway.
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spelling doaj.art-27de7de166c84840a013e810aa2581762023-12-03T13:31:10ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-04-01238446110.3390/ijms23084461Serrated Colorectal Lesions: An Up-to-Date Review from Histological Pattern to Molecular PathogenesisMartino Mezzapesa0Giuseppe Losurdo1Francesca Celiberto2Salvatore Rizzi3Antonio d’Amati4Domenico Piscitelli5Enzo Ierardi6Alfredo Di Leo7Section of Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, ItalySection of Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, ItalySection of Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, ItalySection of Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, ItalySection of Pathology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, ItalySection of Pathology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, ItalySection of Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, ItalySection of Gastroenterology, Department of Emergency and Organ Transplantation, University of Bari, 70124 Bari, ItalyUntil 2010, colorectal serrated lesions were generally considered as harmless lesions and reported as hyperplastic polyps (HPs) by pathologists and gastroenterologists. However, recent evidence showed that they may bear the potential to develop into colorectal carcinoma (CRC). Therefore, the World Health Organization (WHO) classification has identified four categories of serrated lesions: hyperplastic polyps (HPs), sessile serrated lesions (SSLs), traditional serrated adenoma (TSAs) and unclassified serrated adenomas. SSLs with dysplasia and TSAs are the most common precursors of CRC. CRCs arising from serrated lesions originate via two different molecular pathways, namely sporadic microsatellite instability (MSI) and the CpG island methylator phenotype (CIMP), the latter being considered as the major mechanism that drives the serrated pathway towards CRC. Unlike CRCs arising through the adenoma–carcinoma pathway, APC-inactivating mutations are rarely shown in the serrated neoplasia pathway.https://www.mdpi.com/1422-0067/23/8/4461colorectal cancercolorectal serrated lesionssessile serrated lesionsserrated pathwaymicrosatellite instabilityCpG island methylator phenotype
spellingShingle Martino Mezzapesa
Giuseppe Losurdo
Francesca Celiberto
Salvatore Rizzi
Antonio d’Amati
Domenico Piscitelli
Enzo Ierardi
Alfredo Di Leo
Serrated Colorectal Lesions: An Up-to-Date Review from Histological Pattern to Molecular Pathogenesis
International Journal of Molecular Sciences
colorectal cancer
colorectal serrated lesions
sessile serrated lesions
serrated pathway
microsatellite instability
CpG island methylator phenotype
title Serrated Colorectal Lesions: An Up-to-Date Review from Histological Pattern to Molecular Pathogenesis
title_full Serrated Colorectal Lesions: An Up-to-Date Review from Histological Pattern to Molecular Pathogenesis
title_fullStr Serrated Colorectal Lesions: An Up-to-Date Review from Histological Pattern to Molecular Pathogenesis
title_full_unstemmed Serrated Colorectal Lesions: An Up-to-Date Review from Histological Pattern to Molecular Pathogenesis
title_short Serrated Colorectal Lesions: An Up-to-Date Review from Histological Pattern to Molecular Pathogenesis
title_sort serrated colorectal lesions an up to date review from histological pattern to molecular pathogenesis
topic colorectal cancer
colorectal serrated lesions
sessile serrated lesions
serrated pathway
microsatellite instability
CpG island methylator phenotype
url https://www.mdpi.com/1422-0067/23/8/4461
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