Comparative genomic hybridization analysis of genetic alterations in intracranial meningioma

Abstract

Little is known about genetic alterations during malignant progression of meningioma. We have reported our investigation into the genetic pathway underlying the development of intracranial meningioma using comparative genomic hybridization (CGH). Benign meningiomas displayed only a few genetic changes such as monosomy 22. Anaplastic meningiomas manifested more aberrations than typical meningiomas, frequently exhibiting losses of 1p, 2p, 6q, chromosome 10 and 14q, and gain of 20q, in addition to monosomy 22. The average number of alteration sites in each patient with typical meningioma was significantly less than those in each patient with atypical and with anaplastic meningioma. Anaplastic meningiomas showed the chromosomal changes seen in atypical meningiomas together with other aberrations. These CGH findings suggest that losses of 1p, 2p, 6q, chromosome 10 and 14q, and gain of 20q are genetic changes implicated in the malignant progression of meningioma. In this article, we review the studies on CGH in cases of meningioma.