Gastric cancer remains one of the deadliest malignancies worldwide, and progress in therapeutic development has been hindered in part by the limitations of existing animal models. To address this gap, we established a murine model of gastric cancer that closely mirrors the well-characterized Correa cascade driven by Helicobacter pylori infection. Specifically, we utilized the Leb mouse model, which expresses a human-like transgenic ABO/Leb glycosylation pattern in the gastric mucosa, thereby providing a physiologically relevant host environment for H. pylori colonization and disease progression. Using this model, our objective is to elucidate the earliest genetic alterations that arise during the initial phases of gastric carcinogenesis. In this study, we examined the first-ever reported mouse tissue samples of H. pylori–induced gastric cancer. Leb mice were chronically infected with the oncogenic H. pylori strain USU101 (babA⁺, cagA⁺, vacA⁺). Following histopathological confirmation of tumor presence and grading, whole-genome sequencing (WGS) was performed on gastric tumor tissues to characterize somatic mutations associated with malignant transformation. Across two independent experimental cohorts, gastric malignancies developed with an incidence of 67% and 74%, respectively. Gastric cancer was diagnosed in 40% versus 56% of infected Leb mice, while gastric dysplasia was observed in 27% versus 18% of animals in the two series. Histological analyses revealed that the tumors were consistent with intestinal-type gastric adenocarcinoma, and all stages of the Correa cascade - from chronic gastritis to dysplasia and carcinoma - were clearly identified. Notably, the gastric mucosa of H. pylori-infected Leb mice with cancer displayed a threefold increase in inflammatory scores compared with infected mice exhibiting gastritis alone. In contrast, non-infected control mice showed no signs of gastric inflammation or pathological alterations. At this stage, our ongoing work focuses on identifying and mapping the spectrum of mutations present in cancerous gastric tissues, as well as distinguishing background mutations found in infected but non-cancerous mice. These mutation profiles will be systematically compared with those reported in human gastric cancer, with the goal of uncovering conserved genetic events and improving the translational relevance of this model.