Distinct chromosomal aberrations in Epstein-Barr virus-carrying gastric carcinomas tested by comparative genomic hybridization

Background & Aims. Approximately 10% of gastric adenocarcinomas carry the h uman pathogenic Epstein-Barr virus (EBV). The role of EBV in the pathogenes is of these carcinomas remains to be established. Methods: To obtain a comp rehensive overview of chromosomal aberrations in EBV-carrying and EBV-negat ive gastric carcinomas we performed comparative genomic hybridization (CGH) on 44 gastric carcinomas, 10 EBV-positive, and 34 EBV-negative. Additional ly, DNA flow cytometry was done. Results: Loss of chromosome 4p (P < 0.001) and of 11p (P < 0.02) was exclusively restricted to EBV-carrying gastric c arcinomas. In addition, loss of :18q (P < 0.02) was significantly more freq uent in EBV-carrying gastric carcinomas. The latter involves loci, which ha ve already been linked to gastric carcinogenesis such as the DCC and SMAD4 gene. In contrast, the losses on chromosome 4 and JA do not yet harbor a ge ne related to gastric carcinogenesis. No significant correlation was found between DNA-ploidy and the EBV-status. A number of chromosomal aberrations were found at-comparable frequencies in both groups, i.e., losses of chromo some 17, 12q, and loss of 1p. Interestingly, gains of 13q (10/34) and 3q (5 /34) and loss of 1q (5/34) were solely observed in EBV-negative gastric car cinomas. Conclusions: These data indicate that EBV-carrying and EBV-negativ e gastric carcinomas have different pathogenetic pathways in which EBV migh t play a crucial role.