Please use this identifier to cite or link to this item: http://hdl.handle.net/20.500.12857/124561
Title: The molecular landscape of colitis-associated carcinogenesis
Authors: Saraggi, Deborah 
Fassan, Matteo 
Mescoli, Claudia 
Scarpa, Marco 
Valeri, Nicola
Michielan, Andrea 
D'Incá, Renata
Rugge, Massimo 
Keywords: Biomarkers;Colitis;Dysplasia;IBD;Molecular pathology
Keywords Plus: INFLAMMATORY-BOWEL-DISEASE;CHRONIC ULCERATIVE-COLITIS;RAS GENE-MUTATIONS;COLORECTAL-CANCER;MICROSATELLITE INSTABILITY;PRECANCEROUS LESIONS;CROHNS-DISEASE;COLON-CANCER;COLECTOMY SPECIMENS;EPITHELIAL-CELLS
Mesh headings: Adenocarcinoma;Carcinogenesis;Colitis;Colitis, Ulcerative;Colorectal Neoplasms;Precancerous Conditions
Secondary Mesh headings: Adenomatous Polyposis Coli Protein;Biomarkers;Chemokines;Cytokines;DNA Methylation;Disease Progression;Epigenesis, Genetic;Humans;Intestinal Mucosa;Proto-Oncogene Proteins p21(ras);Tumor Suppressor Protein p53
Issue Date: Apr-2017
Publisher: ELSEVIER SCIENCE INC
Journal: Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver 
Abstract: 
In spite of the well-established histopathological phenotyping of IBD-associated preneoplastic and neoplastic lesions, their molecular landscape remains to be fully elucidated. Several studies have pinpointed the initiating role of longstanding/relapsing inflammatory insult on the intestinal mucosa, with the activation of different pro-inflammatory cytokines (TNF-α, IL-6, IL-10, IFN-γ), chemokines and metabolites of arachidonic acid resulting in the activation of key transcription factors such as NF-κB. Longstanding inflammation may also modify the intestinal microbiota, prompting the overgrowth of genotoxic microorganisms, which may act as further cancer promoters. Most of the molecular dysregulation occurring in sporadic colorectal carcinogenesis is documented in colitis-associated adenocarcinoma too, but marked differences have been established in both their timing and prevalence. Unlike sporadic cancers, TP53 alterations occur early in IBD-related carcinogenesis, while APC dysregulation emerges mainly in the most advanced stages of the oncogenic cascade. From the therapeutic standpoint, colitis-associated cancers are associated with a lower prevalence of KRAS mutations than the sporadic variant. Epigenetic changes, including DNA methylation, histone modifications, chromatin remodeling, and non-coding RNAs, are significantly involved in colitis-associated cancer development and progression. The focus now is on identifying diagnostic and prognostic biomarkers, with a view to ultimately designing patient-tailored therapies.
URI: http://hdl.handle.net/20.500.12857/124561
ISSN: 15908658
DOI: 10.1016/j.dld.2016.12.011
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