To clarify the role of human papillomavirus (HPV) and Epstein-Barr virus (EBV) infection in gastric carcinogenesis in relation to overexpression of mutated p53 anti-oncogene, we used PCR to amplify DNA sequences of these viruses and immunohistochemistry to detect p53 overexpression in formaline-fixed, paraffin embedded blocks including 12 normal gastric and 51 gastric carcinoma specimens. HPV and EBV DNA were found in 17% and 0% of normal gastric tissues and in 45% and 27% of gastric carcinoma specimens, respectively. p53 overexpression was shown in 37% of gastric carcinoma specimens only. HPV infection rate was significantly higher in stage I gastric carcinomas as compared with stage IV carcinomas (p<0.03). p53 overexpression was significantly increased in well-differentiated adenocarcinomas as compared with poorly differentiated carcinomas (p<0.01). The rates of both HPV infection and p53 overexpression were significantly higher in gastric carcinomas without vascular invasion than in those with the invasion (p<0.02). No correlation was found between p53 overexpression and/or the presence of viral DNA (HPV/EBV) in regard to the depth of invasion, lymph node involvement, distant metastasis, and the location of the tumors. Our results suggest that some of the gastric carcinomas are associated with HPV and/or EBV infection and p53 mutations, and that all of these may be involved in the early stage of this malignancy. There was no correlation between HPV and or EBV infection and overexpression of p53 in gastric carcinoma.

Related Articles