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Carcinogenesis Advance Access published online on November 4, 2005
Carcinogenesis, doi:10.1093/carcin/bgi244
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© The Author 2005. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received April 29, 2005
Revised September 1, 2005
Accepted October 12, 2005

CANCER BIOLOGY

Genome-wide differences between microsatellite stable and unstable colorectal tumors

Jordi Camps 1, Gemma Armengol 2, Javier del Rey 1, Juanjo Lozano 3, Hanna Vauhkonen 4, Esther Prat 1, Josep Egozcue 1, Lauro Sumoy 3, Sakari Knuutila 4*, and Rosa Miró 1

1 Departament de Biologia Cellular, Fisiologia i Immunologia and Institut de Biotecnologia i de Biomedicina, Universitat Autònoma de Barcelona, Bellaterra, Spain
2 Unitat d'Antropologia, Departament de Biologia Animal, de Biologia Vegetal i d'Ecologia, Universitat Autònoma de Barcelona, Bellaterra, Spain
3 Programa de Bioinformàtica i Genòmica, Centre de Regulació Genòmica (CRG), Barcelona, Spain
4 Department of Pathology, Haartman Institute and HUSLAB, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland

* To whom correspondence should be addressed.
Sakari Knuutila, E-mail: Sakari.Knuutila{at}helsinki.fi


  Abstract

Genomic copy number changes are frequently found in cancers and they have been demonstrated to contribute to carcinogenesis; and it is widely accepted that tumors with microsatellite instability (MSI) are genetically stable and mostly diploid. In the present study we compared the copy number alterations and the gene-expression profiles of microsatellite stable (MSS) and MSI colorectal tumors. A total number of 31 fresh-frozen primary tumors (16 MSS and 15 MSI) were used. Twenty-eight samples (15 MSS and 13 MSI) were analyzed with metaphase comparative genomic hybridization (CGH), nine of which plus one additional sample (4 MSS and 6 MSI) were further analyzed by cDNA-based array CGH. Gene expression analysis was performed with six samples (3 MSS and 3 MSI, four of these used in metaphase CGH analysis) to identify differentially expressed genes possibly located in the lost or amplified regions found by CGH, stressing the biological significance of copy number changes. Metaphase and array CGH analysis of two colon cancer cell lines (HTC116 and SW480, reported as MSI and MSS archetypes) gave comparable results. Alterations found by metaphase CGH in MSS tumors were +20, +8q, -8p and -18q. Interestingly, 1p22, 4q26 and 15q21 were found deleted preferentially in MSS tumors, while 22q13 was found gained in MSI tumors. The regions of alterations identified by array-CGH were gains at 8q24, 16q24.3, and 20q13, and the loss of 5q21, appearing in the both types of tumors. Gene expression analysis revealed genes with specific associations with the copy number changes of the corresponding genomic regions. As a conclusion, colorectal cancer is a heterogeneous disease, demonstrated by the genomic profiles of individual samples. However, our data shows that copy number changes do not occur exclusively in the MSS phenotypes.


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