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[Cancer Research 57, 2860-2864, July 15, 1997]
© 1997 American Association for Cancer Research

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Marked Genetic Differences between Stage pTa and Stage pT1 Papillary Bladder Cancer Detected by Comparative Genomic Hybridization1

Jan Richter2, Feng Jiang2, Jean-Philippe Görög2, Gideon Sartorius2, Carole Egenter, Thomas C. Gasser, Holger Moch, Michael J. Mihatsch and Guido Sauter3

Institute of Pathology [J. R., F. J., J-P. G., G. Sar., C. E., H. M., M. J. M., G. Sau.] and Urological Clinics [T. C. G.], University of Basel, Schonbeinstrasse 40, CH-4003 Basel, Switzerland

Little is known about the genetic changes underlying invasive tumor growth in bladder cancer. Because alterations that are linked to invasive tumor growth may be detectable in minimally invasive (stage pT1) but not in noninvasive (stage pTa) tumors, we searched for genetic differences between 28 pTa and 28 papillary pT1 bladder tumors by comparative genomic hybridization. Losses of 9q (54%), 9p (39%), and Y (28%) and gains of 1q (14%) were most prevalent in pTa tumors. These changes may play a role in the initiation of noninvasive papillary bladder cancer. The total number of aberrations was higher in pT1 tumors (6.5 ± 5.4) than in pTa tumors (2.3 ± 2.1; P = 0.0003), suggesting an increased genetic instability at stage pT1. Specific alterations, which were significantly more frequent in pT1 than in pTa tumors (P ≤ 0.05), included deletions at 2q (36% of pT1 tumros), 8p (32%), and 11p (21%) and gains at 1q (54%), 8q (32%), 3p, 3q, 5p, 6p, and 10p (18% each). These loci are candidates for carrying genes involved in invasive tumor growth in bladder cancer. High-level amplifications at 1q22–24, 3p24–25, 6p22, 8p12, 8q21–22, 10p12.1–14, 11q13, 12q15–21, 13q31–33, Xp11–13, and Xq21–22.2 may pinpoint the location of oncogenes with relevance for bladder cancer.

1 This study was supported by Schweizerische Krebsliga Grant SKL 137-7-1995, Krebsliga Beider Basel, Schweizerischer Nationalfonds Grant NF 3200-043969.95.1, Wilhelm-Sander Stiftung Grant 97.005.1, and Stiftung für Klinische Krebsforschung der Onkologischen Abteilung des Kantonsspitals Basel.

2 These authors have contributed equally to this work.

3 To whom requests for reprints should be addressed.

Received 4/ 4/97. Accepted 5/28/97.




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