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Carcinogenesis Advance Access published online on March 4, 2004
Carcinogenesis, doi:10.1093/carcin/bgh134
© 2004 by Oxford University Press
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© 2004 Oxford University Press

CANCER BIOLOGY

High-resolution analysis of DNA copy number alterations in colorectal cancer by array-based comparative genomic hybridization

Kentaro Nakao 1, Kshama R. Mehta 2, Jane Fridlyand 2, Dan H. Moore 2, Ajay N. Jain 2, Amalia Lafuente 3, John W. Wiencke 4, Jonathan P. Terdiman 2, and Frederic M. Waldman 2*

1 Second Department of Surgery, Showa University School of Medicine, Tokyo, Japan
2 Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA
3 Institut Salut Publica de Catalunya, Universitat de Barcelona, Barcelona, Spain
4 Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA

* Corresponding author. E-mail: waldman{at}cc.ucsf.edu.

Received 2 December 2003 ; revised 9 February 2004 ; accepted 20 February 2004

Abstract

Array-based comparative genomic hybridization (CGH) allows for the simultaneous examination of thousands of genomic loci at 1-2 megabase resolution. Copy number alterations detected by array-based CGH can aid in the identification and localization of cancer causing genes. Here we report the results of array-based CGH in a set of 125 primary colorectal tumors hybridized onto an array consisting of 2463 bacterial artificial chromosome clones. On average, 17.3% of the entire genome was altered in our samples (8.5% ± 6.7% gained and 8.8% ± 7.3% lost). Losses involving 8p, 17p, 18p or 18q occurred in 37%, 46%, 49% and 60% of cases, respectively. Gains involving 8q or 20q were observed 42% and 65% of the time, respectively. A transition from loss to gain occurred on chromosome 8 between 41 and 48 Mb, with 25% of cases demonstrating a gain of 8p11 (45 to 53Mb). Chromosome 8 also contained four distinct loci demonstrating high level amplifications, centering at 44.9, 60, 92.7, and 144.7 Mb. On 20q multiple high level amplifications were observed, centering at 32.3, 37.8, 45.4, 54.7, 59.4, and 65 Mb. Few differences in DNA copy number alterations were associated with tumor stage, location, age and sex of the patient. Microsatellite stable and unstable (MSI-H) tumors differed significantly with respect to the frequency of alterations (20% versus 5% respectively, p<0.01). Interestingly, MSI-H tumors were also observed to have DNA copy number alterations, most commonly involving 8q. This high resolution analysis of DNA copy number alterations in colorectal cancer by array-based CGH allowed for the identification of many small, previously uncharacterized, genomic regions, such as on chromosomes 8 and 20. Array-based CGH was also able to identify DNA copy number changes in MSI-H tumors.

comparative genomic hybridization, colorectal cancer, chromosome 8, chromosome 20, microsatellite instability
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