Epstein-barr virus-associated gastric carcinoma

Abstract

From the first report by MacCarty and Mahle in 1922 [1], gastric carcinoma with lymphoid stroma, characterized by a prominent lymphoid infiltration in the tumor stroma, has been recognized as associated with a favorable prognosis compared with the more common varieties of gastric carcinoma [1-3]. The suggestion was made that the infiltrating lymphocytes might play an important role in immune surveillance and protect against the invading carcinoma cells [4]. These investigations reveal that this specific type of gastric carcinoma might be a separate classification from ordinary gastric carcinoma. In the 1990s, several groups reported that virtually all gastric carcinomas with lymphoid stroma were associated with Epstein-Barr virus (EBV) [5-7]. Furthermore, EBV is also associated with some gastric carcinomas lacking a prominent lymphoid infiltrate [8]. EBV-associated gastric carcinoma (EBVaGC) occurs worldwide. Always a small minority of gastric cancers, the proportion of gastric cancers associated with EBV does not show the profound geographic variation that is characteristic of Burkitt's lymphoma [9]. EBVaGC shows characteristic features in many clinicopathological and genetic studies that differ from the features of gastric carcinoma without EBV, so EBVaGC is appropriately considered a distinct entity. However, in spite of many investigations, the pathogenesis of this tumor remains poorly understood.Advances in virology and molecular biology promise to shed light on this pathway. In this chapter, we review EBVaGC and associated epigenetic changes in the context of current therapy with an eye toward the possibility of targeted therapies in the future. © 2005 Springer-Verlag Tokyo.