Microsatellite instability has been reported in hereditary colorectal cance
r syndrome and in various kinds of human sporadic tumors. it has also been
shown in brain tumors, although with conflicting results. In the present st
udy, DNA samples obtained from 20 primary brain tumors (10 glioblastomas, t
hree 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 differ
ent chromosomes, were used Four of the 20 neoplasias (20%) showed microsate
llite alterations in tumor DNA with respect to normal DNA. Two glioblastoma
s and one atypical meningioma (15%) showed additional bands or bands with s
hift of electrophoretic mobility, whereas allelic loss was observed in two
glioblastomas (10%). In one glioblastoma, one allelic loss and one extra al
lele were observed at two different loci. These data indicate that in prima
ry brain tumors there is not a high genetic instability. Although lye used
markers with inherently high levels of instability, only sporadic microsate
llite alterations were found. Consequently alterations in the mechanisms of
DNA mismatch-repair, the most important cause of replication errors in her
editary and sporadic colorectal cancers, do not seem to play a major role i
n the oncogenesis of primary brain tumors.