Gastric Cancer Origins: Stem Cells, Metaplasia, and Environmental Interactions.

Abstract

The study by Morris and colleagues provides new insights into gastric cancer development, challenging the traditional Correa cascade model. Their findings show that cigarette smoke exposure accelerates dysplasia formation while reducing Helicobacter pylori-associated inflammation and metaplasia. This suggests that dysplasia may arise from tissue-resident stem cells rather than metaplastic cells. The study also supports the idea that metaplasia may play a protective role in maintaining epithelial integrity under chronic stress. These findings contribute to a better understanding of how environmental factors influence gastric carcinogenesis and may help refine approaches to prevention and treatment. See related article by Morris et al., p. 271.