Abstract
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.
Footnotes
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↵1 This work was supported by Sander-Stiftung Grant 93.055.1 (Munich, Germany).
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↵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 September 11, 1995.
- Accepted November 2, 1995.
- ©1995 American Association for Cancer Research.
Volume 55, Issue 24
