Abstract
Epstein‐Barr virus (EBV) infection was studied in a total of 412 patients with poorly differentiated gastric adenocarcinoma by in situ hybridization for EBV‐encoded small RNA. EBV‐speciflc RNA was detected in tumor cell nuclei of 83 (20.1%) of 412 gastric carcinomas, of which 60 were histologically subclassified as gastric carcinoma with lymphoid stroma (GCLS). All EBV‐positive gastric carcinomas as well as 90 randomly selected EBV‐negative gastric carcinomas were further studied for p53 protein expression by immunohistocbemistry. The Overexpression of p53 protein was demonstrated in only 7 (8.4%) of 83 EBV‐positive gastric carcinomas. This was in marked contrast to the frequency of 34.4% in EBV‐negative gastric carcinomas. In addition, a few p53‐positive nuclei were characteristically scattered in the tumors of many EBV‐positive GCLS, but this was not regarded as p53 Overexpression arising from mutation of the gene. Our findings suggested that EBV‐associated gastric carcinomas may arise through a different mechanism from other types of gastric carcinomas without EBV infection.
Keywords: Epstein‐Barr virus, In situ hybridization, p53 protein, Gastric carcinoma with lymphoid stroma
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