Microsatellite instability in primary brain tumors
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Updated: Aug 10, 2026

Processing of Primary Brain Tumor Tissue for Stem Cell Assays and Flow Sorting
Published on: September 25, 2012
E Alvino1, E Fernandez, R Pallini
1Institute of Experimental Medicine, National Council of Research (CNR), Rome, Italy. ester.alvino@ims.rm.cnr.it
Abstract:
Microsatellite instability has been reported in hereditary colorectal cancer syndrome and in various kinds of human sporadic tumors. It has also been shown in brain tumors, although with conflicting results. In the present study, DNA samples obtained from 20 primary brain tumors (10 glioblastomas, three astrocytomas, five meningiomas, one ependymoma, one hemangiopericytoma) were analyzed to detect microsatellite instability. Nine microsatellites, mono, di-, tri- and tetranucleotide repeat markers, located on nine different chromosomes, were used. Four of the 20 neoplasias (20%) showed microsatellite alterations in tumor DNA with respect to normal DNA. Two glioblastomas and one atypical meningioma (15%) showed additional bands or bands with shift of electrophoretic mobility, whereas allelic loss was observed in two glioblastomas (10%). In one glioblastoma, one allelic loss and one extra allele were observed at two different loci. These data indicate that in primary brain tumors there is not a high genetic instability. Although we used markers with inherently high levels of instability, only sporadic microsatellite alterations were found. Consequently, alterations in the mechanisms of DNA mismatch-repair, the most important cause of replication errors in hereditary and sporadic colorectal cancers, do not seem to play a major role in the oncogenesis of primary brain tumors.
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