Header

UZH-Logo

Maintenance Infos

Clinicopathological and molecular specificities of inflammatory bowel disease-related colorectal neoplastic lesions: the role of inflammation


Svrcek, Magali; Borralho Nunes, Paula Maria; Villanacci, Vincenzo; Beaugerie, Laurent; Rogler, Gerhard; De Hertogh, Gert; Tripathi, Monika; Feakins, Roger; H-ECCO group (2018). Clinicopathological and molecular specificities of inflammatory bowel disease-related colorectal neoplastic lesions: the role of inflammation. Journal of Crohn's & Colitis, 12(12):1486-1498.

Abstract

Compared to the general population, patients with inflammatory bowel disease (IBD) have an increased risk of developing colorectal cancer. Molecular mechanisms underlying colorectal carcinogenesis in the setting of IBD are not well understood. However, modern molecular investigative tools have facilitated the identification of features that help distinguish IBD-related carcinoma from sporadic. Moreover, with advances in endoscopic technology and improved understanding of the natural history, the management of colorectal neoplastic lesions in IBD patients has evolved. This review discusses the clinicopathological and molecular features of colorectal neoplastic lesions complicating IBD. Chronic inflammation is believed to promote the development of neoplasia, partly by producing reactive oxygen and nitrogen species (ROS and NOS) which may interact with genes involved in carcinogenetic pathways. Furthermore, alterations in microbiota and in the innate and adaptive immune responses might contribute, particularly by initiating, regulating and sustaining chronic inflammation. Earlier detection and better characterization of neoplastic colorectal lesions complicating IBD and a better knowledge of molecular mechanisms underlying carcinogenesis in this setting should facilitate improvements in the risk stratification of patients with longstanding IBD and in the management of dysplastic and malignant colorectal lesions that arise in this setting.

Abstract

Compared to the general population, patients with inflammatory bowel disease (IBD) have an increased risk of developing colorectal cancer. Molecular mechanisms underlying colorectal carcinogenesis in the setting of IBD are not well understood. However, modern molecular investigative tools have facilitated the identification of features that help distinguish IBD-related carcinoma from sporadic. Moreover, with advances in endoscopic technology and improved understanding of the natural history, the management of colorectal neoplastic lesions in IBD patients has evolved. This review discusses the clinicopathological and molecular features of colorectal neoplastic lesions complicating IBD. Chronic inflammation is believed to promote the development of neoplasia, partly by producing reactive oxygen and nitrogen species (ROS and NOS) which may interact with genes involved in carcinogenetic pathways. Furthermore, alterations in microbiota and in the innate and adaptive immune responses might contribute, particularly by initiating, regulating and sustaining chronic inflammation. Earlier detection and better characterization of neoplastic colorectal lesions complicating IBD and a better knowledge of molecular mechanisms underlying carcinogenesis in this setting should facilitate improvements in the risk stratification of patients with longstanding IBD and in the management of dysplastic and malignant colorectal lesions that arise in this setting.

Statistics

Citations

Dimensions.ai Metrics

Altmetrics

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic for Gastroenterology and Hepatology
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:10 September 2018
Deposited On:30 Nov 2018 12:36
Last Modified:30 Nov 2018 12:38
Publisher:Oxford University Press
ISSN:1873-9946
OA Status:Closed
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1093/ecco-jcc/jjy132
PubMed ID:30202940

Download

Full text not available from this repository.
View at publisher

Get full-text in a library