Open AccessEvidence for Subarachnoid Spread in the Development of Multiple Meningiomas
Author(s) -
Deimling Andreas,
Kraus Jürgen A.,
Stangl Armin P.,
Wellenreuther Ruth,
Lenartz Doris,
Schramm Johannes,
Louis David N.,
Ramesh Vijaya,
Gusella James F.,
Wiestler Otmar D.
Publication year - 1995
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/j.1750-3639.1995.tb00571.x
Subject(s) - exon , neurofibromatosis , meningioma , nonsense mutation , point mutation , neurofibromatosis type 2 , mutation , cancer research , single strand conformation polymorphism , dna sequencing , gene mutation , gene , medicine , biology , pathology , genetics , missense mutation
Meningiomas are among the most common human brain tumors. Occasionally patients develop multiple meningiomas. While it has been surmised that these are multiple primary meningiomas, it is possible that they represent spread of a single primary tumor. Recently, the neurofibromatosis type 2 (NF2) tumor suppressor gene has been shown to carry mutations in meningiomas. In the present study we have analyzed multiple meningiomas from two patients for point mutations in the NF2 gene by SSCP analysis and direct sequencing. We detected point mutations in the meningiomas from both patients. The first patient from which six tumors were available had a three base pair deletion in the splice donor region of exon 7. All tumors showed the identical mutation. The second patient with two independent meningiomas had a nonsense mutation in exon 8 which was the same in both tumors. Analysis of constitutional DNA revealed a wildtype DNA sequence in both cases. There was no family history of neurofibromatosis type 2 in either patient. These data provide strong evidence for a monoclonal origin of multiple meningiomas. Early subarachnoid spread is the most likely mechanism for the formation of these tumors.