Methylation of p16 is an important mechanism in cervical carcinogenesis. However, the relationship between cervical squamous cell carcinoma (SCC) and Epstein-Barr virus (EBV) remains controversial. Here, we explored whether EBV infection and/or p16 gene inactivation would play any role in cervical carcinogenesis. Eighty-two specimens included 41 invasive SCCs, 30 cervical intraepithelial neoplasm (CIN; CIN 1, 11 cases, CIN II, 3 cases, CIN III 16 cases) and 11 nonneoplastic cervices. EBV was detected by polymerase chain reaction (PCR) for EBNA-1 and in situ hybridization for EBER-1. The p16 methylation-status and the expression of p16 protein were studied by methylation-specific PCR and immunohistochemistry, respectively. The materials were divided into four groups: 1) nonneoplastic cervices, 2) CIN I, 3) CIN II-III and 4) invasive SCCs. p16 methylation and p16 immunoexpressions increased in CIN and invasive SCCs than nonneoplastic tissue. p16-methylation and p16-immunoreactivities were higher in the EBV-positive group (p=0.009, p<0.001) than in the EBV-negative group. EBV was detected more frequently in CIN and SCCs than nonneoplastic cervices. In conclusion, a correlation between p16 methylation, p16 immunoreactivity and the detection of EBV strongly suggested that the cooperation of EBV and p16 gene may play a synergic effect on cell cycle deregulation.
Carcinoma, Squamous Cell/genetics/*pathology/virology ; Comparative Study ; Cyclin-Dependent Kinase Inhibitor p16/analysis/*genetics ; *DNA Methylation ; DNA, Viral/genetics/isolation & purification ; Epstein-Barr Virus Infections/genetics/*pathology/virology ; Epstein-Barr Virus Nuclear Antigens/genetics ; Female ; Herpesvirus 4, Human/genetics ; Humans ; Immunohistochemistry ; In Situ Hybridization ; Polymerase Chain Reaction ; Precancerous Conditions/genetics/*pathology/virology ; RNA, Viral/genetics ; Research Support, Non-U.S. Gov't ; Uterine Cervical Neoplasms/genetics/*pathology/virology

OBJECTIVETo study the correlation between hepatitis B virus surface antigen (HBsAg) and hepatitis C virus (HCV) expression as well as fibrosis staging in hepatocellular carcinoma (HCC) and pericarcinomatous tissues.

METHODSThe patterns of HBsAg and HCV in 100 cases of HCC and their surrounding liver tissues were studied on paraffin-embeded sections with immunohistochemistry technique, and liver tissues were also staged.

RESULTSHBV, HCV virus infection were positively correlated with the fibrotic staging (r(s) = 0.32, P = 0.001). HBsAg and HCV were detected both in HCC and pericarcinomatous tissues. The positive rate of HBsAg in Pericarcinomatous Tissues (79%) was higher than that of in HCC tissues (23%). HCV expressions in HCC (15%) and pericarcinomatous tissues (23%) showed no significant differences.

CONCLUSIONThe fibrotic degree in the tissues of liver cancer with previous virus infection was obviously higher than that without virus infection. Viral infection seemed to be one of the reasons causing liver cancer while perennial virusemia would aggravate pathological changes of the liver tissue.

Carcinoma, Hepatocellular ; pathology ; virology ; Hepacivirus ; isolation & purification ; Hepatitis B ; complications ; Hepatitis B Surface Antigens ; isolation & purification ; Hepatitis B virus ; isolation & purification ; Hepatitis C ; complications ; Hepatitis C Antigens ; genetics ; Humans ; Liver ; pathology ; Liver Cirrhosis ; pathology ; Liver Neoplasms ; pathology ; virology ; Precancerous Conditions ; pathology ; virology ; Risk Factors