Introduction

Gastric cancer was the leading cause of cancer-related death worldwide throughout most of the twentieth century, and now ranks second only to lung cancer, with an estimated 950 000 new cases diagnosed annually. The incidence of gastric cancer varies widely in different countries. In the United States, the incidence has dramatically decreased, and in the year 2009, 21 600 new cases are expected to be diagnosed. One of the most important factors implicated in the pathogenesis of gastric cancer is infection with Helicobacter pylori. Studies have shown that this organism is especially adaptable in the hostile gastric environment. An antigen known as CagA, a 120- to 130-kDa protein encoded by cagA genes of H. pylori, interacts directly with host epithelial cells, causing epithelial cell proliferation and ultimately benign gastritis. In more severe cases, a phenotype termed the “gastric cancer phenotype” develops, which is characterized by a predominant pattern of gastritis in the body of the stomach with gastric atrophy and hypochlorhydria. Correa has described in detail the multi-step multifactorial process in the genesis of gastric cancer.

While H. pylori infection is very prevalent, far fewer than 1% of infected individuals will develop gastric cancer. Previous studies have linked H. pylori infection to the overexpression of interleukin-1β (IL-1β). Recent studies using a transgenic mouse model show that IL-1β works by activating myeloid-derived suppressor cells, which are strongly pro-inflammatory. Blocking IL-1β or the myeloid-derived suppressor cells may be a potential strategy for preventing gastric cancer.