ABSTRACT
Gastric cancer is a disease with the second cancer-related mortality in the world. Helicobacter pylori infection that is one of major causes of gastric carcinogenesis induces a chronic inflammation in stomach. The epithelial-mesenchymal transition and/or the accumulation of genetic mutation occur during regenerating the injured gastric epithelial cells due to chronic inflammation by the infection of H. pylori. Normal gastric cells can be transformed into cancer stem cells by the epithelial-mesenchymal transition and/or the accumulation of genetic mutation that initiate the development of gastric cancer. Gastric epithelial cells, bone marrow-derived cells and gastric stem cells in gastric tissue might be the source of gastric cancer stem cells as the target cells that might be susceptible for epithelial-mesenchymal transition and/or the accumulation of genetic mutation. Normal stem cells in gastric tissue regenerating the injured gastric tissue also have the potential to be cancer stem cells known as the origin of cancer development when their ability for regulating differentiation and/or proliferation of normal stem cells is damaged by epithelial-mesenchymal transition and/or the accumulation of genetic mutation. Therefore if the mechanism regulating the transformation of normal stem cells to cancer stem cells is discovered, it might suggest the fundamental therapeutic strategy for preventing the development of gastric cancer by the chronic infection of H. pylori.