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

By means of comparative genomic hybridization (CGH), we screened 58 primary gastric cancers for changes in copy number of DNA sequences, We detected f requent losses on 1p32-33 (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 1p36 (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%), 12p 12-13 (4%), 17q21 (2%), 19q12-13 (2%), and 20q13 (2%). High-level amplification at 8p22-23 has never been reported in any ot her 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 t his exon-like sequence had occurred in all three tumors in which amplificat ions at 8p22-23 had been detected by CGH. Our data provide evidence for sev eral, previously undescribed, genomic aberrations that are characteristic o f gastric cancers, Genes Chromosomes Cancer 24:299-305, 1999. (C) 1999 Wile y-Liss, Inc.