AI Article Synopsis

  • About 10% of meningiomas are aggressive, showing atypical or anaplastic characteristics, while the NF2 tumor suppressor gene plays a key role in their development.
  • Research involving genetically modified mice shows that the loss of specific genes, like Nf2 and p16(Ink4a), increases meningioma formation and allows for the use of MRI to better study and potentially treat these tumors in the future.

Article Abstract

Meningiomas 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 p16(INK4a)/p14(ARF) 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 p16(Ink4a) 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2253711PMC
http://dx.doi.org/10.1111/j.1750-3639.2007.00105.xDOI Listing

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