Comparative genomic hybridization reveals frequent gains of 20q, 8q, 11q, 12p, and 17q, and losses of 18q, 9p, and 15q in pancreatic cancer

✍ Scribed by Eija H. Mahlamäki; Mattias Höglund; Ludmila Gorunova; Ritva Karhu; Sigmund Dawiskiba; Åke Andrén-Sandberg; Olli-P. Kallioniemi; Bertil Johansson

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 111 KB
• Volume: 20
• Category: Article
• ISSN: 1045-2257
• DOI: 10.1002/(sici)1098-2264(199712)20:4<383::aid-gcc10>3.0.co;2-o

✦ Synopsis

Comparative genomic hybridization (CGH) was used to screen for genomic imbalances in 24 exocrine pancreatic carcinomas, including 11 low-passage cell lines (4-8 subcultures) and 13 uncultured samples. Aberrations were found in all cell lines and in seven of the 13 biopsies. The most frequent changes in the cell lines were gains of 20q (91%), 11q (64%), 17q (64%), 19q (64%), 8q, 12p, 14q, and 20p (55%), and losses of 18q (100%), 9p (91%), 15q (73%), 21q (64%), 3p (55%), and 13q (55%). High-level gains (tumor to normal ratio over 1.5) were detected at 3q, 6p, 7q, 8q, 12p, 19q, and 20q. Among the tumor biopsies, overrepresentations of 7p and 8q were most common (31%), followed by 5p, 5q, 11p, 11q, 12p, and 18q (23%), whereas the most frequent losses involved 18p and 18q (31%) and 6q and 17p (23%). The genetic changes in nine samples obtained from metastatic lesions did not differ significantly from those in 15 primary carcinomas. Most of the gains and losses detected in this CGH study correspond well to those identified in previous cytogenetic and molecular genetic investigations of pancreatic carcinomas. However, frequent gain of 12p and loss of 15q have not been previously reported. Molecular genetic analyses of these chromosome arms are warranted, and may lead to the discovery of novel genes important in pancreatic carcinogenesis.