Epstein-Barr virus - Associated gastric carcinomas: Relation to H-pylori infection and genetic alterations

Citation
Ms. Wu et al., Epstein-Barr virus - Associated gastric carcinomas: Relation to H-pylori infection and genetic alterations, GASTROENTY, 118(6), 2000, pp. 1031-1038
Citations number
49
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
GASTROENTEROLOGY
ISSN journal
00165085 → ACNP
Volume
118
Issue
6
Year of publication
2000
Pages
1031 - 1038
Database
ISI
SICI code
0016-5085(200006)118:6<1031:EV-AGC>2.0.ZU;2-R
Abstract
Background & Aims: The association of Epstein-Barr virus (EBV) and gastric carcinomas (GCs) has been shown to vary among different populations and cer tain histological subtypes, Few studies have addressed the status of Helico bacter pylori infection and genetic alterations in these EBV-positive or -n egative GCs. Methods: Eleven gastric lymphoepithelioma-like carcinomas (LEL Cs) and 139 cases of common non-LELCs were evaluated for the presence of EB V DNA using polymerase chain reaction (PCR) and RNA in situ hybridization. H. pylori infection was determined by anti-H. pylori immunoglobulin G in pr eoperative sera. Immunostaining for p53, c-erbB-2, and E-cadherin was perfo rmed. Microsatellite instability was analyzed by PCR using 10 primers. Resu lts: EBV was detected in 11 (100%) LELCs and in 19 (13.7%) of 139 common GC s, Compared with EBV-negative GCs, gastric LELCs tended to have a relativel y higher frequency of proximal location, diffuse histological subtype, p53 overexpression, and reduced E-cadherin expression but a lower frequency of lymph node metastasis, previous H, pylori infection, and c-erbB-2 overexpre ssion. In contrast, no significant difference of clinicopathologic and gene tic profiles was observed between EBV-positive non-LELC GCs and EBV-negativ e GCs, No correlation of microsatellite instability was found among these 3 subsets of GCs, Conclusions: Dissecting clinicopathologic characteristics and infection status of EBV and H, pylori provide additional evidence of et iological and genetic heterogeneity for GC, Distinct clinicopathologic and genetic pathways exist in gastric LELCs, in which EBV may play a more impor tant role than H, pylori infection.