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Comparative Genomic in Situ Hybridization of Colon Carcinomas with Replication Error¹

Institut für Pathologie, Universität Regensburg [J. S., G. S., T. B., J. R., F. H.]; Abteilung für Humanbiologie und Humangenetik, Universität Kaiserslautern [H. S.]; and Chirurgische Universitätsklinik Regensburg [H. Z.], Germany

The aim of the present study was to detect complex genetic alterations in colorectal carcinomas with and without microsatellite instability (MIN) by comparative genomic in situ hybridization. MIN due to replication errors is the hallmark of hereditary nonpolyposis colon cancer. None of 6 MIN-positive tumors showed amplifications, and only 2 tumors displayed deletions of one chromosomal segment each. In contrast, different gains and losses were observed in 11 of 12 MIN-negative carcinomas. The most frequent gains affected chromosomes 7, 13, and 20q, whereas deletions were observed on chromosomes 17, 18, and 9p. These results demonstrate different mechanisms of genetic instability in subgroups of colorectal carcinomas and may, therefore, support the hypothesis of different etiologies in tumors with and without MIN.

¹ This work was supported by Sander-Stiftung Grant 93.055.1 (Munich, Germany).

² Present address: Universitätsklinik, Abteilung Neuropathologie, Baldingerstrasse, D-35033 Marburg, Germany.

³ To whom requests for reprints should be addressed, at Universitätsklinik, Abteilung Neuropathologie, Baldingerstrasse, D-35033 Marburg, Germany. Phone: 49-6421-28-2468; Fax: 49-6421-28-5640; E-mail: stumm@mailer.uni-marburg.de.

Received 9/11/95. Accepted 11/ 2/95.

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