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.
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.
Authors: Maria D Begnami; Andre L Montagnini; Andre L Vettore; Sueli Nonogaki; Mariana Brait; Alex Y Simoes-Sato; Andrea Q A Seixas; Fernando A Soares Journal: World J Gastroenterol Date: 2006-08-21 Impact factor: 5.742
Authors: A Zur Hausen; B P van Rees; J van Beek; M E Craanen; E Bloemena; G J A Offerhaus; C J L M Meijer; A J C van den Brule Journal: J Clin Pathol Date: 2004-05 Impact factor: 3.411
Authors: B G Schneider; S Y Rha; H C Chung; J C Bravo; R Mera; J C Torres; K T Plaisance; R Schlegel; C M McBride; X T Reveles; R J Leach Journal: Mol Pathol Date: 2003-06
Authors: Bastiaan P van Rees; Eric Caspers; Axel zur Hausen; Adriaan van den Brule; Paul Drillenburg; Marian A J Weterman; G Johan A Offerhaus Journal: Am J Pathol Date: 2002-10 Impact factor: 4.307
Authors: Camtu D Truong; Wei Feng; Wei Li; T Khoury; Q Li; S Alrawi; Yingyan Yu; Keping Xie; James Yao; Dongfeng Tan Journal: J Exp Clin Cancer Res Date: 2009-02-03