ROLE OF GENOMIC INSTABILITY IN MENINGIOMA PROGRESSION

Microsatellite length instability, probably resulting from defective D NA mismatch repair mechanisms, has been described in a variety of canc ers. Such genetic instability may play a significant role in tumor for mation and progression. To investigate the role of microsatellite alte rations in meningioma tumorigenesis and progression, we examined 33 mi crosatellite markers on nine chromosomes for abnormalities in 18 benig n, 15 atypical, and 11 malignant meningiomas. In each tumor, at least 15 markers were investigated. Microsatellite instability was not detec ted in any of the cases examined. However, loss of heterozygosity for markers from various chromosomes was seen frequently among atypical an d malignant meningiomas. Although some of these chromosomal losses mig ht represent random events, our data also indicate a role for specific loci on chromosome arms 14(q), 1p, 10q, and possibly 9p in the develo pment of malignancy in meningiomas. Our results argue against a signif icant role for a generalized microsatellite instability phenotype in m eningiomas, but they suggest that genomic instability resulting in fre quent allelic deletions may contribute to meningioma progression. (C) 1996 Wiley-Liss, Inc.