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dc.contributor.authorKalamarides, Michel
dc.contributor.authorStemmer-Rachamimov, Anat
dc.contributor.authorTakahashi, Masaya
dc.contributor.authorHan, Zhi-Yan
dc.contributor.authorChareyre, Fabrice
dc.contributor.authorNiwa-Kawakita, Michiko
dc.contributor.authorBlack, Peter McLaren
dc.contributor.authorCarroll, Rona Stephanie
dc.contributor.authorGiovannini, Marco
dc.date.accessioned2011-04-18T02:55:53Z
dc.date.issued2008
dc.identifier.citationKalamarides, Michel, Anat O. Stemmer-Rachamimov, Masaya Takahashi, Zhi-Yan Han, Fabrice Chareyre, Michiko Niwa-Kawakita, Peter M. Black, Rona S. Carroll, and Marco Giovannini. 2008. Natural History of Meningioma Development in Mice Reveals: A Synergy of Nf2 and p16Ink4a Mutations. Brain Pathology (Zurich, Switzerland) 18(1): 62-70.en_US
dc.identifier.issn1015-6305en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:4853408
dc.description.abstractMeningiomas account for approximately 30% of all primary central nervous system tumors and are found in half of neurofibromatosis type 2 patients often causing significant morbidity. Although most meningiomas are benign, 10% are classified as atypical or anaplastic, displaying aggressive clinical behavior. Biallelic inactivation of the neurofibromatosis 2 (NF2) tumor suppressor is associated with meningioma formation in all NF2 patients and 60% of sporadic meningiomas. Deletion of the p16INK4a/p14ARF locus is found in both benign and malignant meningiomas, while mutation of the p53 tumor suppressor gene is uncommon. Previously, we inactivated Nf2 in homozygous conditional knockout mice by adenoviral Cre delivery and showed that Nf2 loss in arachnoid cells is rate-limiting for meningioma formation. Here, we report that additional nullizygosity for p16Ink4a increases the frequency of meningioma and meningothelial proliferation in these mice without modifying the tumor grade. In addition, by using magnetic resonance imaging (MRI) to screen a large cohort of mutant mice, we were able to detect meningothelial proliferation and meningioma development opening the way to future studies in which therapeutic interventions can be tested as preclinical assessment of their potential clinical application.en_US
dc.language.isoen_USen_US
dc.publisherBlackwell Publishing Ltden_US
dc.relation.isversionofdoi:10.1111/j.1750-3639.2007.00105.xen_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2253711/pdf/en_US
dash.licenseLAA
dc.titleNatural History of Meningioma Development in Mice Reveals: A Synergy of Nf2 and p16Ink4a Mutationsen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalBrain Pathology (Zurich, Switzerland)en_US
dash.depositing.authorStemmer-Rachamimov, Anat
dc.date.available2011-04-18T02:55:53Z
dash.affiliation.otherHMS^Pathologyen_US
dash.affiliation.otherHMS^Surgery-Children's Hospitalen_US
dash.affiliation.otherHMS^Surgery-Children's Hospitalen_US
dash.affiliation.otherHMS^Medicine-Brigham and Women's Hospitalen_US
dc.identifier.doi10.1111/j.1750-3639.2007.00105.x*
dash.contributor.affiliatedStemmer-Rachamimov, Anat
dash.contributor.affiliatedCarroll, Rona
dash.contributor.affiliatedBlack, Peter


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