Surface markers of gastric cancer stem cells

The integrity of the gastric epithelium is maintained by the gastric stem cells, which proliferate and selfrenew, giving rise to transient amplifying cells that replace the constantly renewing epithelium. Since in rapidly renewing organs like the stomach, stem cells live long enough to accumulate the multiple genetic changes required for transformation, it is postulated that resident stem cells may, in a chronically inflamed environment, accumulate a series of genetic and epigenetic changes over time that lead to the emergence of gastric cancer stem cells. Alternatively, the setting of chronic inflammatory stress may lead to loss of the indigenous gastric stem cells from their niches, followed by recruitment and engraftment of bone marrow derived stem cells into the gastric epithelium, thus contributing to gastric cancer. Recently, gastric stem cell responses after Helicobacter pylori (H. pylori) infection and recruitment of bone marrow derived stem cells to the inflammatory site have been reported. Despite the tremendous efforts made to identify markers to isolate gastric cancer stem cells, hitherto, only two molecules have been shown to be promising as marker progenitors: villin and Lgr5. This review highlights the advances in the identification of surface markers of gastric cancer stem cells, with emphasis on the effect of H. pylori infection on the stem cell compartment.