Novel chromosomal aberrations in a recurrent malignant meningioma

The molecular basis of tumorigenesis and tumor progression in meningiomas is not fully understood. Here we present results of conventional cytogenetic, fluorescence in situ hybridization (FISH), and comparative genetic hybridization (CGH) analyses in a patient with recurrent anaplastic meningioma. We found complex aberrant karyotype alterations previously described in anaplastic meningiomas, such as 1p, 14q aberration, and a possibly tetraploid karyotype. Loss of chromosome 22q was detected by conventional cytogenetic analysis. Additional chromosomal aberrations not previously reported included a near-triploid karyotype and alterations such as 4p+, 5p−, 7p+, 8q+, and gain of chromosome 19. FISH with LSI 9p21, CEP9, LSI PML/RARA, and CGH confirmed the karyotype complexity in this case. Our findings of several previously unreported cytogenetic alterations suggest that complex karyotype alterations are a characteristic feature in anaplastic meningiomas. High chromosomal complexity might be associated with a highly aggressive meningioma phenotype.