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Comparative genomic hybridization (CGH) provides a new possibility for the investigation of genetic alterations in tumour genomes. In our experiments CGH was carried out using genomic DNA from human glioblastoma multiforme (GBM) as a probe for chromosomal in situ suppression hybridization. Amplified DNA sequences contained in the tumour DNA showed specific signals, revealing the chromosomal positions of these sequences. Using this approach we detected amplifications of different chromosomal segments in individual GBM specimens. In accordance with the results from Southern analysis demonstrating amplification of the EGFR gene in 45% of human GBM, CGH signals in different GBM mapped to the region of this gene on chromosome 7p. Other signals detected by CGH involved chromosome 12q and 8q. Our data demonstrate CGH as a novel comprehensive and rapid approach for the analysis of complex genomic alterations in glial tumours.

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.