Lkb1-deficient mice developed gastric polyps similar to those previously described [42], the onset of which was 270 days after induction Mice were killed shortly after this point and no bladder tumours were observed in these animals.
These mice developed gastric polyps and adenocarcinoma of the stomach and small intestine [ 8].
About half of mice with heterozygous deletion of ELF developed hepatocellular carcinoma, and 90% of ELF+/−/Smad4+/− mice developed gastric cancer and other gastrointestinal cancers [ 23, 24].
Importantly, K19-Wnt1 mice developed gastric tumours at 20 weeks after H. felis infection, whereas no tumours were found in the H. felis-infected wild-type mice.
25 Surprisingly, A4gnt null mice developed gastric adenocarcinoma through a hyperplasia dysplasia carcinoma sequence in the absence of H. pylori infection.
Seventy six percent of 48-wk H. felis-infected bak-null mice developed gastric corpus dysplasia, whereas only 25% of control C57BL/6 animals that were infected at the same time developed dysplastic glands.
25 An INS-GAS mouse develops gastric metaplasia, dysplasia, carcinoma and gastric cancer with vascular invasion at 20 months of age; this model shows a direct link between gastrin and gastric cancer.
In mouse models, gp130F/F mice spontaneously develop gastric inflammation and intestinal-type gastric tumors [ 69]. gp130 is IL-6 family receptor signaling subunit, and IL-6 family gp130 driver IL-11 drives hyperactivation of STAT3 contributing gastric phenotype.
Transgenic mice that develop gastric tumors present suitable models to decipher gastric tumorigenesis, and identify novel therapeutic targets.
Levanon and colleagues questioned the causal relationship between loss of RUNX3 expression and gastric cancer, and reported that RUNX3-deficient mice did not develop gastric hyperplasia or gastric tumors [ 20, 21].
