Researchers created mice with a stable mutation in the β-catenin gene to study its role in intestinal tumorigenesis. By using embryonic stem cells, they generated a mutant allele where exon 3, containing phosphorylation sites, was flanked by loxP sequences. When crossed with mice expressing Cre recombinase in the intestines, this led to the deletion of exon 3, resulting in stabilized β-catenin. This caused the formation of intestinal adenomatous polyps, similar to those seen in ApcΔ716 knockout mice. The study showed that activation of the Wnt signaling pathway through stabilized β-catenin can lead to intestinal and colonic tumors. The results provide direct experimental evidence that Wnt signaling is involved in intestinal tumorigenesis. The study also found that the mutant β-catenin protein was expressed in intestinal polyps but not in normal epithelium, and that the polyps were more irregular and heterogeneous in size compared to those in ApcΔ716 knockout mice. The study also showed that the mutant β-catenin protein was present in the colon, but no conspicuous polyps were found there. The study concluded that the Wnt signaling pathway is involved in intestinal tumorigenesis mediated by β-catenin. The research provides important insights into the role of β-catenin in intestinal tumorigenesis and the mechanisms underlying the development of intestinal polyps.Researchers created mice with a stable mutation in the β-catenin gene to study its role in intestinal tumorigenesis. By using embryonic stem cells, they generated a mutant allele where exon 3, containing phosphorylation sites, was flanked by loxP sequences. When crossed with mice expressing Cre recombinase in the intestines, this led to the deletion of exon 3, resulting in stabilized β-catenin. This caused the formation of intestinal adenomatous polyps, similar to those seen in ApcΔ716 knockout mice. The study showed that activation of the Wnt signaling pathway through stabilized β-catenin can lead to intestinal and colonic tumors. The results provide direct experimental evidence that Wnt signaling is involved in intestinal tumorigenesis. The study also found that the mutant β-catenin protein was expressed in intestinal polyps but not in normal epithelium, and that the polyps were more irregular and heterogeneous in size compared to those in ApcΔ716 knockout mice. The study also showed that the mutant β-catenin protein was present in the colon, but no conspicuous polyps were found there. The study concluded that the Wnt signaling pathway is involved in intestinal tumorigenesis mediated by β-catenin. The research provides important insights into the role of β-catenin in intestinal tumorigenesis and the mechanisms underlying the development of intestinal polyps.