Identification of frequent chromosomal aberrations in ductal adenocarcinoma of the pancreas by comparative genomic hybridization (CGH)

✍ Scribed by Schleger, Christiane; Arens, Norbert; Zentgraf, Hanswalter; Bleyl, Uwe; Verbeke, Caroline

• Publisher: John Wiley and Sons
• Year: 2000
• Tongue: English
• Weight: 99 KB
• Volume: 191
• Category: Article
• ISSN: 0022-3417
• DOI: 10.1002/(sici)1096-9896(200005)191:1<27::aid-path582>3.0.co;2-j

✦ Synopsis

Despite the continuous progress in molecular methodology, the genetic events involved in the initiation and progression of ductal adenocarcinoma of the pancreas remain largely unknown. In this study, 33 pancreatic ductal adenocarcinomas were screened for genomic alterations by comparative genomic hybridization (CGH). To date, most CGH studies of pancreatic cancer have been based on cell lines. To emphasize genetic imbalances that are involved in the in vivo development and progression of pancreatic carcinoma only fresh-frozen or paraf®n-embedded tumour samples were analysed in the present study. Twenty-two tumours (67%) showed genomic alterations involving up to three (12%) or more (55%) chromosomal regions. The number and nature of the genetic imbalances did not, however, correlate with tumour stage or grade. Chromosome 18 was preferentially altered in the tumours analysed. Frequent chromosomal losses were found at 18q, 10q, 8p, and 13q. Commonly gained regions were located on 8q and 3q. Moreover, high copy number ampli®cations of the chromosomal regions 5p, 8q22-ter, 12p12-cen, 19q12±13.2, and 20q were identi®ed. These data provide evidence for the occurrence of characteristic genomic alterations which are of biological relevance for the genesis of pancreatic cancer. The identi®ed altered chromosomal regions may harbour tumour genes which involved in the multistep process of pancreatic carcinogenesis.