Abstract:

Epstein-Barr virus-associated gastric carcinoma (EBVaGC) is a distinct subtype that accounts for nearly 10% of gastric carcinomas. This type of gastric cancer has no relation to any mutation in chromosomal genes, and EBV causes cancer by affecting the epigenetics of host cells through methylation and inactivation of the promoter of tumor suppressor genes. This suggests that EBV infection precedes the clonal growth of EBV-infected cells and subsequently develops carcinoma. Chronic gastritis in the background of EBVaGC might enhance the chance of interaction between gastric epithelial cells and B lymphocytes, and cytokines produced by inflammatory cells might support the growth of EBV-infected gastric epithelial cells. Numerous modifiable risk factors have been identified for gastric cancer (GC). Inflammation is a complicated host immune response to biological, chemical, and physical invasions. Chronic inflammation, which is caused by genetic mutations, autoimmune diseases, constant exposure to environmental factors, and viral infections, can significantly increase the risk of cancer. According to epidemiologic studies, chronic infection and inflammation are considered the main risk factors for different types of cancer. Furthermore, although oncogenic viruses stimulate inflammation by dint of different mechanisms, they generally activate certain signaling pathways, including NF-κB and STAT3, in charge of cancer development. The role of EBV in chronic gastric inflammation has received little attention. However, several studies have indicated EBV as well as Helicobacter pylori to be initially involved in the oncogenic process of gastric cancer by increasing chronic inflammation and tissue damage. Moreover, other risk factors including lifestyle and HPV infection play a role in the progress of gastric cancer.

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