Epstein-Barr virus infection and p16(INK4a) overexpression in gastric adenocarcinoma.
- Author:
Ping WANG
1
;
Qing ZHANG
;
Jin-Feng YANG
;
Ze-Nong CHENG
;
Ke ZHANG
;
Dong-Hong YU
Author Information
- Publication Type:Journal Article
- MeSH: Adenocarcinoma; genetics; metabolism; pathology; virology; Adult; Aged; Cyclin-Dependent Kinase Inhibitor p16; genetics; metabolism; Epstein-Barr Virus Infections; genetics; metabolism; pathology; virology; Female; Gene Expression Regulation, Neoplastic; Herpesvirus 4, Human; genetics; metabolism; Humans; Male; Middle Aged; Neoplasm Staging; Stomach Neoplasms; genetics; metabolism; pathology; virology; Viral Matrix Proteins; genetics; metabolism
- From: Chinese Journal of Experimental and Clinical Virology 2008;22(4):244-246
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study Epstein-Barr virus infection and p16 protein abnormal expresson in carcinogenesis and progression of gastric adenocarcinomas (GAC).
METHODSImmunohistochemical staining SP method was used to detect the expression of LMP-1 and p16 in 97 cases of GAC.
RESULTSEBV LMP-1 and p16 protein were detected in 30.9% (30/97) and in 63.91% (62/97) cases of gastric adenocarcinomas respectively. There was no significant difference between EBV-positive and EBV-negative gastric carcinomas in sex, histologic type, depth of tumor invision, lymph node metastasis and clinical stages (P > 0.05); overexpression of p16 was associated with lymph node metastasis and clinical stages; no correlation was found between the expression of EBV LMP-1 and p16 protein.
CONCLUSION1. EBV play a role in carcinogensis of GAC. 2. P16 gene abnormality is frequently involved in GAC and might be one of the important prognostic factors. 3. EBV infection and p16 alteration are two independent roles in GAC carcinogenesis.
