Allelic gain and amplification on the long arm of chromosome 17 in anaplastic meningiomas

Brain Pathol. 2002 Apr;12(2):145-53. doi: 10.1111/j.1750-3639.2002.tb00429.x.


Using comparative genomic hybridization (CGH) we have previously identified amplification at 17q21-qter as a common aberration in anaplastic meningiomas but not in atypical or benign meningiomas (19). To define the amplified genomic region, we analyzed 44 meningeal tumors, including 7 benign meningiomas of World Health Organization (WHO) grade 1,19 atypical meningiomas (WHO grade II) and 18 anaplastic meningiomas (WHO grade III) at 46 chromosome 17 loci (including 42 17q loci). In line with the CGH data we found evidence of increased numbers of alleles on 17q. The incidence rose with malignancy grade, culminating at 61% (11 of 18 cases) in the anaplastic meningioma group. The majority of cases showing increased allele numbers had, on average, low-level allelic gains (relative increase in allele dosage of 2- to 5-fold). Amplification of alleles (defined here as an average relative increase in allele dosage of more than 5 times) was detected in 2 anaplastic meningiomas. The amplification patterns in these tumors defined a number of common regions of amplification/increased allele copy number, the best defined include one between D17S790 and D17S1607 and one between D17S1160 and PS6K. Real-time PCR analysis of the PS6K candidate gene revealed no high-level amplification despite this affecting adjacent loci. Our findings are fundamental for the identification of the gene(s) in 17q22-q23 that is (are) the target(s) for increased copy number in anaplastic meningiomas and possibly other tumor types.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • Aged, 80 and over
  • Alleles*
  • Child
  • Chromosomes, Human, Pair 17 / genetics*
  • Female
  • Gene Amplification*
  • Humans
  • Male
  • Meningeal Neoplasms / genetics*
  • Meningioma / genetics*
  • Microsatellite Repeats / genetics
  • Middle Aged
  • Nucleic Acid Hybridization
  • Ribosomal Protein S6 Kinases / genetics


  • Ribosomal Protein S6 Kinases