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Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-48396

Cattaneo, E; Laczko, E; Buffoli, F; Zorzi, F; Bianco, M A; Menigatti, M; Bartosova, Z; Haider, R; Helmchen, B; Sabates-Bellver, J; Tiwari, A; Jiricny, J; Marra, G (2011). Preinvasive colorectal lesion transcriptomes correlate with endoscopic morphology (polypoid vs. nonpolypoid). EMBO Molecular Medicine, 3(6):334-347.

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Abstract

Improved colonoscopy is revealing precancerous lesions that were frequently missed in the past, and ∼30% of those detected today have nonpolypoid morphologies ranging from slightly raised to depressed. To characterize these lesions molecularly, we assessed transcription of 23,768 genes in 42 precancerous lesions (25 slightly elevated nonpolypoid and 17 pedunculated polypoid), each with corresponding samples of normal mucosa. Nonpolypoid versus polypoid morphology explained most gene expression variance among samples; histology, size, and degree of dysplasia were also linked to specific patterns. Expression changes in polypoid lesions frequently affected cell-cycling pathways, whereas cell-survival dysregulation predominated in nonpolypoid lesions. The latter also displayed fewer and less dramatic expression changes than polypoid lesions. Paradigmatic of this trend was progressive loss through the normal > nonpolypoid > polypoid > cancer sequence of TMIGD1 mRNA and protein. This finding, along with TMIGD1 protein expression patterns in tissues and cell lines, suggests that TMIGD1 might be associated with intestinal-cell differentiation. We conclude that molecular dysregulation in slightly elevated, nonpolypoid, precancerous colorectal lesions may be somewhat less severe than that observed in classic adenomatous polyps.

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Molecular Cancer Research
07 Faculty of Science > Institute of Molecular Cancer Research
DDC:570 Life sciences; biology
Language:English
Date:2011
Deposited On:16 Jun 2011 11:38
Last Modified:27 Nov 2013 20:29
Publisher:Wiley-Blackwell
ISSN:1757-4676
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:10.1002/emmm.201100141
PubMed ID:21538994
Citations:Web of Science®. Times Cited: 9
Google Scholar™
Scopus®. Citation Count: 9

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