Mapping of chromosomal imbalances in pancreatic carcinoma by comparative genomic hybridization

S Solinas-Toldo, C Wallrapp, F Müller-Pillasch… - Cancer research, 1996 - AACR
S Solinas-Toldo, C Wallrapp, F Müller-Pillasch, M Bentz, T Gress, P Lichter
Cancer research, 1996AACR
To identify recurrent chromosomal imbalances in pancreatic adenocarcinoma, 27 tumors
were analyzed by using comparative genomic hybridization. In 23 cases chromosomal
imbalances were found. Gains of chromosomal material were much more frequent than
losses. The most common overrepresentations were observed on chromosomes 16p (eight
cases), 20q (seven cases), 22q (six cases), and 17q (five cases) and underrepresentations
on a subregion of chromosome 9p (eight cases). Distinct high-level amplifications were …
Abstract
To identify recurrent chromosomal imbalances in pancreatic adenocarcinoma, 27 tumors were analyzed by using comparative genomic hybridization. In 23 cases chromosomal imbalances were found. Gains of chromosomal material were much more frequent than losses. The most common overrepresentations were observed on chromosomes 16p (eight cases), 20q (seven cases), 22q (six cases), and 17q (five cases) and underrepresentations on a subregion of chromosome 9p (eight cases). Distinct high-level amplifications were found on 1p32-p34, 6q24, 7q22, 12p13, and 22q. These data provide evidence for a number of new cytogenetically defined recurrent aberrations which are characteristic of pancreatic carcinoma. The overrepresented or underrepresented chromosomal regions represent candidate regions for potential oncogenes and tumor suppressor genes, respectively, possibly involved in pancreatic tumorigenesis.
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