Original Paper Summary We evaluated the rate of Epstein-Barr virus (EBV) in- fection in gastric carcinomas of Korean patients and in- vestigated the associations between EBV infection and clinicopathological characteristics, the survival rates of patients, and p53 overexpression. EBV-encoded small RNA (EBER)-in situ hybridization and immunohisto- chemistry for p53 protein were done in 306 consecutive gastric carcinoma cases, of which 17 (5.6%) showed EBV infection. Of these 17 EBV-positive cases, one case strongly expressed p53 protein, while 98 (34%) of 285 EBV-negative cases overexpressed p53 (p < 0.05). The EBV-positive gastric carcinomas tended to have lymphoid stroma. They were mostly of the poorly dif- ferentiated type, negative for p53 immunoexpression, more prevalent in male patients, and diffuse according to Lauren’s classification (p < 0.05). There was no sig- nificant difference in the survival rate for the EBV sta- tus. In conclusion, the EBV infection rate among gastric carcinomas in Korea is similar to that ascertained in other countries. An inverse correlation between EBV and p53 overexpression was disclosed. Further study is needed to find out whether or not two genetic changes could be functionally overlapping during gastric car- cinogenesis. Key words: Stomach neoplasms – Human herpesvirus 4 – Epstein-Barr virus – In situ hybridization – Protein p53 Introduction The Epstein-Barr virus (EBV) is a ubiquitous human herpes virus implicated in the etiology of many human Clinicopathologic Characteristics of Epstein-Barr Virus-Incorporated Gastric Cancers in Korea M ee Soo Chang 1 , Hye Seung Lee 1 , Chul Woo Kim 1 , Yong Il Kim 1 , and Woo Ho Kim 1, 2 1 Department of Pathology and 2 Cancer Research Institute, Seoul National University College of Medicine, Seoul, Korea Pathol. Res. Pract. 197: 395–400 (2001) 0344-0338/01/197/6-395 $15.00/0 PATHOLOGY RESEARCH AND PRACTICE © Urban & Fischer Verlag http://www.urbanfischer.de/journals/prp lymphoid [5] and epithelial malignancies. The presence of EBV DNA in gastric carcinomas was first document- ed in 1990 using the polymerase chain reaction [3]. As the EBV-encoded small RNA (EBER) is considered a unique marker of latent infection, and EBERs are found in high concentration (10 6 –10 7 copies/cell) in EBV-as- sociated gastric cancer cells [15], EBV infection in gas- tric cancer is considered a latent state. There is some ev- idence supporting the etiologic association between EBV and gastric carcinoma in patients with EBV-posi- tive gastric carcinoma. Firstly, in situ hybridization re- veals that the EBV gene product is uniformly present in all carcinoma cells [8, 24]. Secondly, Southern blot hy- bridization of the EBV terminal repeat fragment dis- closed that the EBV DNA in a carcinoma cell is mono- clonal [13, 24]. Finally, there is serological evidence of high antiviral titers, especially of EBV viral-capsid anti- gen IgA and EBV early antigen R component IgG, many years before the diagnosis of EBV-positive gas- tric carcinoma [19]. The mechanism by which EBV contributes to the carcinogenesis of the gastric mucosa is still unknown. It has been thought that EBV-induced clonal proliferation promotes the malignant transformation by increasing the chance of oncogenic changes, and EBV is required to maintain the malignant phenotype of EBV-associated gastric malignancies [6, 14, 20, 23, 26, 31]. EBV-associated gastric carcinoma occurs worldwide, with varying degrees of incidence in different countries. Although there is some controversy about the EBV in- Address for correspondence: Woo Ho Kim, Department of Pathology, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul 110- 799, Korea. Tel: +82-2-740-8269, Fax: +82-2-765-5600, E-mail: woohokim@snu.ac.kr