Comprehensive modeling of the Correa cascade in precancerous lesions of gastric cancer: Leveraging animal, cellular, and organoid systems for translational insights

Figure 3 Commonly used strategies for constructing animal models of precancerous lesions of gastric cancer. Including: (1) Chemical carcinogen-induced models using agents such as N-methyl-N’-nitro-N-nitrosoguanidine or N-Nitroso-N-methylurea in combination with high-salt diet, ethanol, bile acids, or sodium deoxycholate; (2) Infection-based models using Helicobacter pylori in mice or Mongolian gerbils to mimic inflammation-driven transformation; (3) Combination models integrating chemical exposure with Helicobacter pylori infection, high-salt feeding, ethanol administration, fasting, or ammonia water to accelerate disease progression; and (4) Spasmolytic polypeptide-expressing metaplasia models induced by tamoxifen, L635, or DMP-777, which recapitulate key features of gastric glandular cell transdifferentiation. DCA: Deoxycholic acid; CDCA: Chenodeoxycholic acid; MNNG: N-methyl-N’-nitro-N-nitrosoguanidine; MNU: N-Nitroso-N-methylurea; H. pylori: Helicobacter pylori; S. anginosus: Streptococcus anginosus; H. felis: Helicobacter felis; Trx1: Thioredoxin 1; SD: Sprague-Dawley.