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

Citation
C. Schleger et al., Identification of frequent chromosomal aberrations in ductal adenocarcinoma of the pancreas by comparative genomic hybridization (CGH), J PATHOLOGY, 191(1), 2000, pp. 27-32
Citations number
24
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF PATHOLOGY
ISSN journal
00223417 → ACNP
Volume
191
Issue
1
Year of publication
2000
Pages
27 - 32
Database
ISI
SICI code
0022-3417(200005)191:1<27:IOFCAI>2.0.ZU;2-#
Abstract
Despite the continuous progress in molecular methodology, the genetic event s involved in the initiation and progression of ductal adenocarcinoma of th e pancreas remain largely unknown. In this study, 33 pancreatic ductal aden ocarcinomas were screened for genomic alterations by comparative genomic hy bridization (CGH), To date, most CCH 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 paraffin-embedded tumour samples were analysed in the present stu dy. Twenty-two tumours (67%) showed genomic alterations involving up to thr ee (12%) or more (55%) chromosomal regions. The number and nature of the ge netic imbalances did not, however, correlate with tumour stage or grade. Ch romosome 18 was preferentially altered in the tumours analysed. Frequent ch romosomal losses were found at 18q, 10q, 8p, and 13q. Commonly gained regio ns were located on 8q and 3q, Moreover, high copy number amplifications of the chromosomal regions 5p, 8q22-ter, 12p12-cen, 19q12-13.2, and 20q were i dentified. These data provide evidence for the occurrence of characteristic genomic alterations which are of biological relevance for the genesis of p ancreatic cancer. The identified altered chromosomal regions may harbour tu mour genes which involved in the multistep process of pancreatic carcinogen esis. Copyright (C) 2000 John Wiley & Sons, Ltd.