Distinct chromosomal aberrations of ampulla of Vater and pancreatic head cancers detected by laser capture microdissection and comparative genomic hybridization
Journal
Oncology Reports
Journal Volume
14
Journal Issue
4
Pages
867-872
Date Issued
2005
Author(s)
Abstract
Despite the continuous progress in molecular methodology, the genetic events involved in the carcinogenesis of pancreatic head ductal carcinomas (PHDCs) and ampulla of Vater cancer (AVC) remain largely unknown. Their proximity within the confined region lends them to very similar clinical presentations and operative approaches. However, it is unclear why AVC has a significantly better outcome than PHDCs. The drastic difference may arise from the distinct tumor origins. Therefore, the study of genetic alterations within these two neighboring tumors may elucidate their mechanisms. However, previous genetic analysis of PHDCs may have been influenced by contamination of excessive stromal and inflammatory cells in the background. To date, most comparative genomic hybridization (CGH) studies of pancreatic cancer are based in cell lines or specimens that were not microdissected. Even AVC has a paucity of data. To determine the differences of the genetic alterations of PHDCs and AVC, we used laser capture microdissection combined with degenerated oligonucleotide polymerase chain reaction and CGH to identify the chromosomal aberrations. Frequent gains were found on 5p, 13q, 3q, 8q, 1p, 2p, 2q, 3q, 7p, 8p, 9p, 13q, and 21q, while frequent losses were located on 7p, 18q, 1p, 11q, 16q, 19q, 1q, 2q, 3p, 19p, and 17p in PHDCs. In AVC, chromosomal gains occurred frequently in 7p, 8q, 1q, 2q, 3p, 4p, 7p, 3q, 5p, 20p, 20q, 4q, 5q, 7q, 11p, 12p, 13q, 14q, 18p, 18q, 21q, 9p, 10p, and 15q, and losses frequently in 17q, 1p, 18q, 19p, 5q, 10p, and 10q. This is the first report on the CGH profiles of AVC. These data provide evidence that chromosomal gains/amplifications of AVC differ from those of PHDCs. Among them, chromosomal gains on 1q25, 7p15, 8q23, and 3p21, and losses on 17q24, were statistically higher in AVC than PHDCs (p<0.05). The gains and losses suggest possible putative tumor suppressors and oncogenes that may be involved in the different carcinogenic pathways of AVC.
SDGs
Other Subjects
DNA; adult; aged; article; bile duct tumor; chromosome; chromosome aberration; female; genetics; human; image processing; laser; male; metabolism; middle aged; nucleic acid hybridization; pancreas tumor; tumor cell line; ultrastructure; Vater papilla; Adult; Aged; Ampulla of Vater; Cell Line, Tumor; Chromosome Aberrations; Chromosomes; Common Bile Duct Neoplasms; DNA; Female; Humans; Image Processing, Computer-Assisted; Lasers; Male; Middle Aged; Nucleic Acid Hybridization; Pancreatic Neoplasms
Type
journal article