ArticleJournal of neurology, neurosurgery, and psychiatry2000
Low frequency of replication errors in primary nervous system tumours.
Article in Journal of neurology, neurosurgery, and psychiatry, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 24 citations in OpenAlex.
- Mismatch Repair Pathway, Genome Stability and Cancer.Frontiers in molecular biosciences · 2020Review
- Molecular Genetics of Intracranial Meningiomas with Emphasis on Canonical Wnt Signalling.Cancers · 2016Review
- Microsatellite instability in pediatric high grade glioma is associated with genomic profile and differential target gene inactivation.PloS one · 2011Article
- Low-level microsatellite instability phenotype in sporadic glioblastoma multiforme.Journal of cancer research and clinical oncology · 2005Article
- mtDNA mutations in tumors of the central nervous system reflect the neutral evolution of mtDNA in populations.Oncogene · 2004Article
- Multiplexed analysis of post-PCR fluorescence-labeled microsatellite alleles and statistical evaluation of their imbalance in brain tumors.Japanese journal of cancer research : Gann · 2002Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesAutomated 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 (chi(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.
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