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[Cancer Research 63, 2872-2880, June 1, 2003]
© 2003 American Association for Cancer Research

Molecular Biology and Genetics

Array-based Comparative Genomic Hybridization for Genome-Wide Screening of DNA Copy Number in Bladder Tumors1

Joris A. Veltman, Jane Fridlyand, Sunanda Pejavar, Adam B. Olshen, James E. Korkola, Sandy DeVries, Peter Carroll, Wen-Lin Kuo, Daniel Pinkel, Donna Albertson, Carlos Cordon-Cardo, Ajay N. Jain and Frederic M. Waldman2

Cancer Center [J. F., S. P., A. B. O., J. E. K., S. D., W-L. K.]; and Departments of Laboratory Medicine [D. P., D. A., A. N. J., F. M. W.] and Urology [P. C.], University of California-San Francisco, San Francisco, California 94143-0808; Department of Human Genetics, University Medical Center Nijmegen, Nijmegen, the Netherlands [J. A. V.]; and Department of Epidemiology and Biostatistics [A. B. O.] and Department of Pathology [C. C-C.], Memorial Sloan-Kettering Cancer Center, New York, New York

Genome-wide copy number profiles were characterized in 41 primary bladder tumors using array-based comparative genomic hybridization (array CGH). In addition to previously identified alterations in large chromosomal regions, alterations were identified in many small genomic regions, some with high-level amplifications or homozygous deletions. High-level amplifications were detected for 192 genomic clones, most frequently at 6p22.3 (E2F3), 8p12 (FGFR1), 8q22.2 (CMYC), 11q13 (CCND1, EMS1, INT2), and 19q13.1 (CCNE). Homozygous deletions were detected in 51 genomic clones, with four showing deletions in more than one case: two clones mapping to 9p21.3 (CDKN2A/p16, in nine cases), one at 8p23.1 (three cases), and one at 11p13 (two cases). Significant correlations were observed between copy number gain of clones containing CCNE1 and gain of ERBB2, and between gain of CCND1 and deletion of TP53. In addition, there was a significant complementary association between gain of CCND1 and gain of E2F3. Although there was no significant relationship between copy number changes and tumor stage or grade, the linked behavior among genomic loci suggests that array CGH will be increasingly important in understanding pathways critical to bladder tumor biology.




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