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Quantitative
Analysis of Neurofibromatosis Type 2 Gene Transcripts in Meningiomas Supports
the Concept of Distinct Molecular Variants |
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Ruth Wellenreuther,
Andreas Waha, Ylin Vogel, Doris Lenartz, Johannes Schramm, Otmar Dieter
Wiestler, and Andreas von Deimling |
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Department
of Neuropathology (RW, AW, YV, ODW, AvD), University of Bonn Medical Center,
Bonn; Department of Neurosurgery (DL), Hospital Cologne-Merheim, Cologne;
and Department of Neurosurgery (JS), University of Bonn Medical Center,
Bonn, Germany |
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Meningiomas frequently show
mutational inactivation of the neurofibromatosis type 2 tumor suppressor
gene (NF2 gene). In a previous study, mutations were preferentially observed
in the fibroblastic and transitional subtypes (75%), whereas the meningothelial
variant was significantly less affected (25%). To study a potential role
of the NF2 gene on the transcriptional level, we have analyzed NF2 transcripts
in 67 meningiomas of different subtypes. A competitive reverse transcriptase-PCR
assay with an external NF2 gene standard was used for quantitative mRNA
analysis. Fibroblastic and transitional meningiomas exhibited significantly
lower levels of NF2 mRNA compared with meningothelial variants (p = 0.001,
unpaired t test). These data support the concept of a distinct molecular
pathway in the formation of meningothelial meningiomas independent from
the NF2 gene or its gene product merlin/schwannomin. In addition, in these
tumors, NF2 expression was reduced by a factor of 10 (p < 0.001, unpaired
t test) in those meningiomas with NF2 gene mutations suggesting decreased
stability or impaired transcription of mutated NF2 mRNA. In conclusion,
our data provide further evidence for molecular differences between subtypes
of meningiomas and support an NF2-independent pathogenesis of meningothelial
meningiomas. |
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