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Frequent gain of copy number on the long arm of chromosome 20 in human pancreatic adenocarcinoma
Author(s) -
Fukushige Shinichi,
Waldman Frederic M.,
Kimura Mitsuhiro,
Abe Tadayoshi,
Furukawa Toru,
Sunamura Makoto,
Kobari Masao,
Horii Akira
Publication year - 1997
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199707)19:3<161::aid-gcc5>3.0.co;2-w
Subject(s) - biology , comparative genomic hybridization , chromosome , fluorescence in situ hybridization , carcinogenesis , pancreatic cancer , genetics , microbiology and biotechnology , gene duplication , adenocarcinoma , chromosome 17 (human) , gene , cancer research , cancer
We have used comparative genomic hybridization (CGH) to survey genomic regions with aberrant copy numbers of DNA sequences in pancreatic adenocarcinoma. In 12 cell lines and 6 primary tumors from 18 patients with pancreatic adenocarcinomas, highly frequent losses (>60%) were observed on chromosome arms 6q, 9p, and 18q and the Y chromosome. Moderately frequent losses (40–60%) were observed on chromosome arms 3p, 4q, 8p, and 21q. Interestingly, these samples showed extremely high frequencies of increases in copy numbers of DNA sequences on the long arm of chromosome 20 (15/18, 83%). We further analyzed five cell lines by fluorescence in situ hybridization (FISH) with probes on chromosome 20 to define the increase in copy number more accurately, and we found that 20q was increased to between 5 and 8 copies per cell. These results suggest the existence of an oncogene or oncogenes on 20q that play a role in the development and/or the progression of pancreatic carcinogenesis. Genes Chromosom. Cancer 19:161–169, 1997. © 1997 Wiley‐Liss Inc.