Nf2 gene inactivation in arachnoidal cells is rate-limiting for meningioma development in the mouse

Michel Kalamarides, Michiko Niwa-Kawakita, Hélène Leblois, Vincent Abramowski, Michel Perricaudet, Anne Janin, Gilles Thomas, David H. Gutmann, Marco Giovannini

Research output: Contribution to journalArticlepeer-review

175 Scopus citations

Abstract

Biallelic NF2 gene inactivation is common in sporadic and in neurofibromatosis type 2 (NF2)-related meningiomas. We show that, beginning at four months of age, thirty percent of mice with arachnoidal cell Cre-mediated excision of Nf2 exon 2 developed a range of meningioma subtypes histologically similar to the human tumors. Additional hemizygosity for p53 did not modify meningioma frequency or progression suggesting that Nf2 and p53 mutations do not synergize in meningeal tumorigenesis. This first mouse model initiated with a genetic lesion found in human meningiomas provides a powerful tool for investigating tumor progression and for the preclinical evaluation of therapeutic interventions.

Original languageEnglish
Pages (from-to)1060-1065
Number of pages6
JournalGenes and Development
Volume16
Issue number9
DOIs
StatePublished - May 1 2002

Keywords

  • Adenoviral vector
  • Conditional knockout mice
  • Cre/loxP
  • Meningioma
  • NF2
  • Tumor suppressor gene

Fingerprint

Dive into the research topics of 'Nf2 gene inactivation in arachnoidal cells is rate-limiting for meningioma development in the mouse'. Together they form a unique fingerprint.

Cite this