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
Frequent amplification of 8q24, 11q, 17q, and 20q-specific genes in pancreatic cancer
✍ Scribed by Eija H. Mahlamäki; Maarit Bärlund; Minna Tanner; Ludmila Gorunova; Mattias Höglund; Ritva Karhu; Anne Kallioniemi
- Book ID
- 102844881
- Publisher
- John Wiley and Sons
- Year
- 2002
- Tongue
- English
- Weight
- 576 KB
- Volume
- 35
- Category
- Article
- ISSN
- 1045-2257
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✦ Synopsis
Abstract
Genetic changes involved in the development and progression of pancreatic cancer are still partly unknown, despite the progress in recent years. In this study, comparative genomic hybridization analysis in 31 pancreatic cancer cell lines showed that chromosome arms 8q, 11q, 17q, and 20q are frequently gained in this tumor type. Copy number analysis of selected genes from these chromosome arms by fluorescence in situ hybridization showed amplification of the MYC oncogene in 54% of the cell lines, whereas CCND1 was amplified in 28%. In the 17q arm, the ERBB2 oncogene was amplified in 20% of the cell lines, TBX2 in 50%, and BIRC5 in 58%, indicating increased involvement toward the q telomere of chromosome 17. In the 20q arm, the amplification frequencies varied from 32% to 83%, with the CTSZ gene at 20q13 being most frequently affected. These results illustrate that amplification of genes from the 8q, 11q, 17q, and 20q chromosome arms is common in pancreatic cancer. © 2002 Wiley‐Liss, Inc.
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