Low frequency of replication errors in primary nervous system tumours
Maria Jesús Sobridoa c, Carlos Rodriguez Pereirab, Francisco Barrosc, Jerónimo Fortezab, Ángel Carracedoc, Manuela Lemaa
a Department of
Neurology, Complexo Hospitalario Universitario de Santiago, Santiago de
Compostela, Spain, b Department of Pathology, c Molecular Medicine Unit,
FINGO, Hospital de Conxo
Correspondence to: Dr M J Sobrido, Neurogenetics Programme, UCLA Department of Neurology, 710 Westwood Plaza, Los Angeles, CA 90095, USA msobrido{at}ucla.edu
Received 4 November
1999 and in revised form 20 March 2000;
Accepted 6 April
2000
OBJECTIVES
Automated
DNA technology was used to analyze the incidence of microsatellite
instability (MIN) among the most frequent types of adult primary CNS
tumours and to determine its relation with clinicopathological characteristics.
METHODSFifty six
gliomas, 32 meningiomas and 11 schwannomas were screened for size
changes at eight microsatellite loci using fluorescent polymerase chain
reaction (PCR) followed by fragment analysis in an automated sequencer.
A tumour was considered as MIN+ when a different electrophoretic
pattern between constitutional and tumour DNA was evidenced in one or
more microsatellite markers and as replication error positive (RER+)
when at least 25% of the markers analyzed (2/8) showed instability.
The MIN phenotype was correlated with relevant clinical and
pathological parameters.
RESULTSGlobally,
instability was found in 19/767 analyses (2.47%), with a higher rate
among tetranuceotide than dinucleotide repeats (
2 test,
p=0.018). Ten gliomas (17.9%), two meningiomas (6.3%), and two
schwannomas (18.2%) were MIN+, whereas one glioma (1.8%), two
meningiomas (6.3%), and one schwannoma (9.1%) were classified as
RER+. A possible association between microsatellite instability and a
shorter duration of clinical course was found in meningiomas. The MIN+
phenotype was more frequent in spinal than intracranial schwannomas
(Fisher's exact test, p=0.018). No other significant association with
clinical or histological features was detected.
CONCLUSIONSAlthough
microsatellite instability can be demonstrated at a low rate in some
primary CNS tumours, a true replication error phenotype (revealed by
widespread microsatellite instability at numerous loci) is uncommon and
unlikely to play an important part in the pathogenesis of these
neoplasms. This form of instability was more frequent in
tetranucleotide than in dinucleotide repeats. To our knowledge, this is
the first report of MIN in schwannomas, where it was associated with
the spinal localisation of the tumour.
Keywords: microsatellite instability; central nervous system tumours; automated DNA analysis
© 2000 by Journal of Neurology, Neurosurgery, and Psychiatry
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