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Yoshiaki Ito, Cancer Science Institute, National University of Singapore, Center for Translational Medicine, Singapore,
Khay Guan Yeoh, Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore and National University Health System, Singapore
Although the worldwide incidence of gastric cancer has declined in recent years, it is still the second most frequent cause of cancer-related death in the world.
Environmental factors play critical roles in the pathogenesis of gastric cancer, with the major risk factors being Helicobacter pylori (H. pylori) infection, diet, and smoking (1). H. pylori infection is the most important single risk factor for gastric cancer development and has been defined as a Class 1 carcinogen by the World Health Organization (WHO). Populations with high incidences of gastric cancer can be found in geographic areas with high prevalence of H. pylori infection. High salt intake, often due to traditional diet in the form of salted fish, is the best-documented dietary risk factor for atrophic gastritis (2).
Epstein–Barr virus (EBV) infection is correlated with Burkitt’s lymphoma in Africa and nasopharyngeal carcinoma in South-East Asia. In addition, this virus has been recognized as an etiological agent in 5–10% of gastric cancers (3). Infectious agents, therefore, play important causative roles in gastric carcinogenesis.
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