Transcriptional analysis of left-sided colitis, pancolitis, and ulcerative colitis-associated dysplasia

Détails

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Etat: Serval
Version: Final published version
ID Serval
serval:BIB_52238F1DD46D
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Transcriptional analysis of left-sided colitis, pancolitis, and ulcerative colitis-associated dysplasia
Périodique
Inflammatory Bowel Diseases
Auteur(s)
Bjerrum J.T., Nielsen O.H., Riis L.B., Pittet V., Mueller C., Rogler G., Olsen J.
ISSN
1536-4844 (Electronic)
ISSN-L
1078-0998
Statut éditorial
Publié
Date de publication
2014
Peer-reviewed
Oui
Volume
20
Numéro
12
Pages
2340-2352
Langue
anglais
Notes
Journal Article Publication Status: ppublish IUMSP2014/12
Résumé
BACKGROUND: It is unknown why patients with extensive ulcerative colitis (UC) have a higher risk of colorectal cancer compared with patients with left-sided UC. This study characterizes the inflammatory processes in left-sided UC, pancolitis, and UC-associated dysplasia at the transcriptional level to identify potential biomarkers and transcripts of importance for the carcinogenic behavior of chronic inflammation.
METHODS: The Affymetrix GeneChip Human Genome U133 Plus 2.0 was applied on colonic biopsies from UC patients with left-sided UC, pancolitis, dysplasia, and controls. Reverse transcription polymerase chain reaction and immunohistochemistry were performed for validating selected transcripts in the initial cohort and in 2 independent cohorts of patients with UC. Microarray data were analyzed by principal component analysis, and reverse transcription polymerase chain reaction and immunohistochemistry data by the Wilcoxon's rank-sum test.
RESULTS: The principal component analysis results revealed separate clusters for left-sided UC, pancolitis, dysplasia, and controls. Close clustering of dysplastic and pancolitic samples indicated similarities in gene expression. Indeed, 101 and 656 parallel upregulated and downregulated transcripts, respectively, were identified in specimens from dysplasia and pancolitis. Validation of selected transcripts hereof identified insulin receptor alpha (INSRA) and MAP kinase interacting serine/threonine kinase 2 (MKNK2) with an enhanced expression in dysplasia compared with left-sided UC and controls, whereas laminin γ2 (LAMC2) was found with a lower expression in dysplasia compared with the remaining 3 groups.
CONCLUSIONS: This study demonstrates pancolitis and left-sided UC as distinct inflammatory processes at the transcriptional level, and identifies INSRA, MKNK2, and LAMC2 as potential critical transcripts in the inflammation-driven preneoplastic process of UC.
Pubmed
Web of science
Création de la notice
25/11/2014 10:06
Dernière modification de la notice
03/03/2018 17:12
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