Single nucleotide polymorphism array profiling identifies distinct chromosomal aberration patterns across colorectal adenomas and carcinomas

Zarzour, Peter, Boelen, Lies, Luciani, Fabio, Beck, Dominik, Sakthianandeswaren, Anuratha, Mouradov, Dmitri, Sieber, Oliver M., Hawkins, Nicholas J., Hesson, Luke B., Ward, Robyn L. and Wong, Jason W. H. (2015) Single nucleotide polymorphism array profiling identifies distinct chromosomal aberration patterns across colorectal adenomas and carcinomas. Genes Chromosomes Cancer, 54 5: 303-314. doi:10.1002/gcc.22243

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Author Zarzour, Peter
Boelen, Lies
Luciani, Fabio
Beck, Dominik
Sakthianandeswaren, Anuratha
Mouradov, Dmitri
Sieber, Oliver M.
Hawkins, Nicholas J.
Hesson, Luke B.
Ward, Robyn L.
Wong, Jason W. H.
Title Single nucleotide polymorphism array profiling identifies distinct chromosomal aberration patterns across colorectal adenomas and carcinomas
Journal name Genes Chromosomes Cancer   Check publisher's open access policy
ISSN 1045-2257
1098-2264
Publication date 2015-02-27
Year available 2015
Sub-type Article (original research)
DOI 10.1002/gcc.22243
Volume 54
Issue 5
Start page 303
End page 314
Total pages 12
Place of publication Hoboken, NJ, United States
Publisher John Wiley & Sons
Collection year 2016
Language eng
Abstract The progression of benign colorectal adenomas into cancer is associated with the accumulation of chromosomal aberrations. Even though patterns and frequencies of chromosomal aberrations have been well established in colorectal carcinomas, corresponding patterns of aberrations in adenomas are less well documented. The aim of this study was to profile chromosomal aberrations across colorectal adenomas and carcinomas to provide a better insight into key changes during tumor initiation and progression. Single nucleotide polymorphism array analysis was performed on 216 colorectal tumor/normal matched pairs, comprising 60 adenomas and 156 carcinomas. While many chromosomal aberrations were specific to carcinomas, those with the highest frequency in carcinomas (amplification of chromosome 7, 13q, and 20q; deletion of 17p and chromosome 18; LOH of 1p, chromosome 4, 5q, 8p, 17p, chromosome 18, and 20p) were also identified in adenomas. Hierarchical clustering using chromosomal aberrations revealed three distinct subtypes. Interestingly, these subtypes were only partially dependent on tumor staging. A cluster of colorectal cancer patients with frequent chromosomal deletions had the least favorable prognosis, and a number of adenomas (n = 9) were also present in the cluster suggesting that, at least in some tumors, the chromosomal aberration pattern is determined at a very early stage of tumor formation. Finally, analysis of LOH events revealed that copy-neutral/gain LOH (CN/G-LOH) is frequent (>10%) in carcinomas at 5q, 11q, 15q, 17p, chromosome 18, 20p, and 22q. Deletion of the corresponding region is sometimes present in adenomas, suggesting that LOH at these loci may play an important role in tumor initiation.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ
Additional Notes Published online ahead of print 27 February 2015.

Document type: Journal Article
Sub-type: Article (original research)
Collections: Office of the Vice-Chancellor
Official 2016 Collection
School of Medicine Publications
 
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Created: Thu, 05 Mar 2015, 22:25:55 EST by Robyn Ward on behalf of Office of Deputy Vice-Chancellor (Research)