Genetic alterations of gastric cancer: Comparative genomic hybridization and fluorescence in situ hybridization studies

Genetic changes leading to the development of gastric cancers are still in dispute. In the following study, we used comparative genomic hydridization (CGH) to screen for DNA copy number following study, we used comparative genomic hybridization (CGH) to screen for DNA copy number changes along all chromosomes in 37 gastric carcinomas, and fluorescence in situ hybridization (FISH) with the C-MYC and TP53 probes in 14 cases for comparison. The aim of this study was to identify those chromosome regions that contain genes important for the development of gastric carcinomas and to identify genetic markers associated with tumor progression. The most often involved gains were 2q, 7pq, 8pq, 13q, 17q, 18q, and 20pq. The most commonly deleted regions were 17p. The pattern of genetic changes was different depending on the existence of nodal metastasis and histologic types. Gains in 8q and losses in 17p were the most common features of the CGH changes. However, only 3 among the available 10 cases (30%) showed an amplification of the C-MYC gene by FISH. Allelic loss of TP53 was found in 2 of 4 cases (50%). This difference might be due to another rearrangement of these 2 genes which cannot be detected by FISH, or other possible genesis and nodal metastasis of gastric carcinomas. genes in that area may be involved in the tumorigenesis and nodal metastasis of gastric carcinomas. (C) Elsevier Science Inc. 2000. All rights reserved.