Gains, losses, and amplifications of genomic materials in primary gastric cancers analyzed by comparative genomic hybridization

✍ Scribed by Chouhei Sakakura; Toshiki Mori; Tomoya Sakabe; Yoji Ariyama; Takashi Shinomiya; Kosei Date; Akeo Hagiwara; Toshiharu Yamaguchi; Toshio Takahashi; Yusuke Nakamura; Tatsuo Abe; Johji Inazawa

• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 242 KB
• Volume: 24
• Category: Article
• ISSN: 1045-2257
• DOI: 10.1002/(sici)1098-2264(199904)24:4<299::aid-gcc2>3.0.co;2-u

✦ Synopsis

By means of comparative genomic hybridization (CGH), we screened 58 primary gastric cancers for changes in copy number of DNA sequences. We detected frequent losses on Ip32-33 (21%), 3p21-23 (22%), 5q14-22 (36%), 6q16 (26%), 9p21-24 (22%), 16q (21%), 17p13 (48%), 18q11-21(33%), and 19(40%). Gains were most often noted at I p36 (22%), 8p22-23 (24%), 8q23-24 (29%), 11q12-13 (24%), 16p(21%), 20p (38%), 20q (45%), Xp21-22(38%), and Xq21-23 (43%), with high-level amplifications at 6p21(2%),7q31(10%), 8p22-23(5%), 8q23-24 (7%), 11q13(4%), 12p12-13(4%), 17q21(2%), 19q12-13(2%), and 20q13(2%). High-level amplification at 8p22-23 has never been reported in any other cancer type and its frequency was as high as that reported for the MYC, MET, and KRAS genes. We narrowed down the smallest common amplicon to 8p23.1 by reverse-painting FISH to prophase chromosomes. Southern blot analysis using one EST marker (D38736) clearly demonstrated that amplification of this exon-like sequence had occurred in all three tumors in which amplifications at 8p22-23 had been detected by CGH. Our data provide evidence for several, previously undescribed, genomic aberrations that are characteristic of gastric cancers.