Expression of stabilized β-catenin in differentiated neurons of transgenic mice does not result in tumor formation

John E. Kratz, Duncan Stearns, David L. Huso, Hilda H. Slunt, Donald L. Price, David R. Borchelt, Charles G. Eberhart

Research output: Contribution to journalArticlepeer-review

Abstract

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 β-catenin in the brain. Methods: Wild-type and mutant human β-catenin transgenes were expressed under the control of a murine PrP promoter fragment that drives high level postnatal expression in the CNS. Mutant β-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 β-catenin protein levels in the cortex and cerebellum of adult animals. Immunohistochemical analysis revealed nuclear β-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 β-catenin, suggesting that postnatal Wnt signaling in differentiated neurons may not be sufficient to induce CNS tumorigenesis.

Original languageEnglish (US)
Article number33
JournalBMC cancer
Volume2
DOIs
StatePublished - Dec 2 2002

ASJC Scopus subject areas

  • Genetics
  • Oncology
  • Cancer Research

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