PRESENCE OF HIGH-LEVEL DNA COPY NUMBER GAINS IN GASTRIC-CARCINOMA ANDSEVERELY DYSPLASTIC ADENOMAS BUT NOT IN MODERATELY DYSPLASTIC ADENOMAS

Our aim was to investigate the presence of DNA copy number changes in gastric adenomas and to identify the changes that may play a role in g astric carcinogenesis. DNA copy number changes in 16 patients with gas tric adenoma and in 22 tumors from patients with intestinal type gastr ic carcinomas were studied by using comparative,genomic hybridization. DNA copy number changes were found in 44% of the adenoma cases and in 86% of the intestinal type gastric carcinomas. On average, gains were more common than losses (0.9 vs. 0.5 in adenomas and 4.1 vs. 1.8 in c arcinomas). In adenomas, the most common gains involved chromosome 8 i n 3 cases, and gain of chromosome 7 and 20q was detected in 2 cases. T he most frequent losses were observed at 5q (three times). Only adenom as with severe dysplasia showed high-level amplifications that were de tected at chromosome 13, 17cen-q22, and 20q12-ter. In gastric cancer, the most common gains were detected at 20q (55%), 17q12-q21 (41%), and 8q (41%), and the most common losses were detected at 18q (43%) and 4 q (32%). High-level amplifications were observed at 20q (3 tumors), 17 cen-q21 (3 tumors), 2p (1 tumor), and 18q (1 tumor). These findings su ggest that the progression of dysplasia is associated with higher leve ls of DIVA copy number increase (e.g., the gains at 17q and 20q), whic h were typically observed in the intestinal type gastric cancer. Furth ermore, the results support the hypothesis that adenoma precedes cance r. (C) Elsevier Science Inc., 1998.