Homozygous deletions of the CDKN2/p16 gene in dural hemangiopericytomas |
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Authors: | Yasuhiro Ono Keisuke Ueki J T Joseph D N Louis |
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Institution: | (1) Molecular Neuro-Oncology Laboratory, CNY6, Neurosurgical Service and Department of Pathology, Massachusetts General Hospital-East and Harvard Medical School, 149 13th St., Charlestown, MA 02129, USA Tel: 1-617-726-5510; Fax: 1-617-726-5079, US;(2) Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA, US |
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Abstract: | While most authors currently classify dural-based hemangiopericytoma (HPC) as a distinct entity rather than as a subtype
of meningioma, the histogenesis of HPC has long been debated. We have recently shown that meningiomas contain frequent mutations
of the neurofibromatosis 2 gene, while HPCs do not, suggesting that HPC is genetically distinct from meningioma. In the present
study, we evaluated a series of 31 dural HPCs (including 3 pairs of primary and recurrent tumor) and 26 meningiomas for alterations
in the cell-cycle regulatory genes CDKN2/p16 and p53. Homozygous deletions of the CDKN2/p16 gene were detected using a comparative
multiplex polymerase chain reaction assay in 7 of 28 primary HPCs (25%), but in only one of 26 meningiomas (P = 0.03). Among the HPCs with recurrence, 1 pair of 3 had a homozygous CDKN2/p16 deletion. The 1 meningioma with a CDKN2/p16
deletion was a meningothelial meningioma, without atypical or malignant features. Single-strand conformational polymorphism
analysis of all three exons of CDKN2/p16 and exons 5–8 of p53 revealed no mutations in either HPCs or meningiomas. These results
illustrate that homozygous deletions of CDKN2/p16 occur in HPCs and suggest that alterations of the p16-mediated cell-cycle
regulatory pathway may underlie the formation or progression of some HPCs. The data also provide further genetic evidence
that HPC is not a subtype of meningioma.
Received: 26 September 1995 / Revised, accepted: 30 October 1995 |
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Keywords: | CDKN2 Hemangiopericytoma Meningioma p16 p53 |
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