Distinct chromosomal aberrations in epstein-barr virus-carrying gastric carcinomas tested by comparative genomic hybridization

Axel Zur Hausen, Nicole C.T. Van Grieken, Gerrit A. Meijer, Mario A.J.A. Hermsen, Elisabeth Bloemena, Stefan G.M. Meuwissen, Jan P.A. Baak, Chris J.L.M. Meijer, Ernst J. Kuipers, Adriaan J.C. Van den Brule

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Background & Aims: Approximately 10% of gastric adenocarcinomas carry the human pathogenic Epstein-Barr virus (EBV). The role of EBV in the pathogenesis of these carcinomas remains to be established. Methods: To obtain a comprehensive overview of chromosomal aberrations in EBV-carrying and EBV-negative gastric carcinomas we performed comparative genomic hybridization (CGH) on 44 gastric carcinomas, 10 EBV-positive, and 34 EBV-negative. Additionally, 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 carcinomas. In addition, loss of 18q (P < 0.02) was significantly more frequent in EBV-carrying gastric carcinomas. The latter involves loci, which have already been linked to gastric carcinogenesis such as the DCC and SMAD4 gene. In contrast, the losses on chromosome 4 and 11 do not yet harbor a gene 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 chromosome 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 carcinomas. Conclusions: These data indicate that EBV-carrying and EBV-negative gastric carcinomas have different pathogenetic pathways in which EBV might play a crucial role.

Original languageEnglish
Article number90207
Pages (from-to)612-618
Number of pages7
JournalGastroenterology
Volume121
Issue number3
DOIs
Publication statusPublished - 2001

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