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Role of genomic instability in meningioma progression

✍ Scribed by Matthias Simon; Andrew J. Kokkino; Ronald E. Warnick; John M. Tew Jr.; Andreas von Deimling; Anil G. Menon

Publisher
John Wiley and Sons
Year
1996
Tongue
English
Weight
468 KB
Volume
16
Category
Article
ISSN
1045-2257

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✦ Synopsis

Microsatellite length instability, probably resulting from defective DNA mismatch repair mechanisms, has been described in a variety of cancers. Such genetic instability may play a significant role in tumor formation and progression. To investigate the role of microsatellite alterations in meningioma tumorigenesis and progression, we examined 33 microsatellite markers on nine chromosomes for abnormalities in I8 benign, I5 atypical, and I I malignant meningiomas. In each tumor, at least I5 markers were investigated. Microsatellite instability was not detected in any of the cases examined. However, lots of heterozygosity for markers from various chromosomes was seen frequently among atypical and malignant meningiomas. Although some of these chromosomal losses might represent random evems, our data also indicate a role for specific loci on chromosome arms 14q, I p, I Oq. and possibly 9p in the development of malignancy in meningiomas. Our results argue against a significant role for a generalized microsatellite instability phenotype in meningiomas, but they suggest that genomic instability resulting in frequent allelic deletions may contribute to meningioma progression. Genes Chromosom Cancer 16965-269 ( I 996).

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