Abstract
Helicobacter pylori (H. pylori) infection drives gastric cancer through chronic inflammation. Here, we present a protocol for establishing a mouse model that induces persistent gastritis and tumorigenesis through chronic ethanol feeding after H. pylori eradication, recapitulating persistent gastritis and precancerous and cancerous phenotypes. We describe steps for H. pylori infection, triple-drug eradication therapy, and ethanol administration. Subsequent tissue collection, histopathology, and molecular analyses assess inflammation and tumor development, enabling investigation of how post-eradication inflammation and alcohol exposure synergistically promote gastric carcinogenesis For complete details on the use and execution of this protocol, please refer to Aziz et al.1.