| First Author | Kratz JE | Year | 2002 |
| Journal | BMC Cancer | Volume | 2 |
| Pages | 33 | PubMed ID | 12460454 |
| Mgi Jnum | J:80326 | Mgi Id | MGI:2445665 |
| Doi | 10.1186/1471-2407-2-33 | Citation | Kratz JE, et al. (2002) Expression of stabilized beta-catenin in differentiated neurons of transgenic mice does not result in tumor formation. BMC Cancer 2(1):33 |
| abstractText | BACKGROUND: Medulloblastomas, embryonal tumors arising in the cerebellum, commonly contain mutations that activate Wnt signaling. To determine whether increased Wnt signaling in the adult CNS is sufficient to induce tumor formation, we created transgenic mice expressing either wild-type or activated beta-catenin in the brain. METHODS: Wild-type and mutant human beta-catenin transgenes were expressed under the control of a murine PrP promoter fragment that drives high level postnatal expression in the CNS. Mutant beta-catenin was stabilized by a serine to phenylalanine alteration in codon 37. RESULTS: Expression of the mutant transgene resulted in an approximately two-fold increase in beta-catenin protein levels in the cortex and cerebellum of adult animals. Immunohistochemical analysis revealed nuclear beta-catenin in hippocampal, cortical and cerebellar neurons of transgenic animals but not in non-transgenic controls. Tail kinking was observed in some transgenic animals, but no CNS malformations or tumors were detected. CONCLUSIONS: No tumors or morphologic alterations were detected in the brains of transgenic mice expressing stabilized beta-catenin, suggesting that postnatal Wnt signaling in differentiated neurons may not be sufficient to induce CNS tumorigenesis. |
