ArticlePloS one2011
Microsatellite instability in pediatric high grade glioma is associated with genomic profile and differential target gene inactivation.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 52 citations in OpenAlex.
- Nivolumab with or without ipilimumab in pediatric patients with high-grade CNS malignancies: Safety, efficacy, biomarker, and pharmacokinetics-CheckMate 908.Neuro-oncology · 2023Trial
- Mismatch Repair Deficiency in Gliomas: A Rare Insight into Microsatellite Instability and Its Diagnostic Implications.Asian journal of neurosurgery · 2025Article
- Unveiling MMR deficiency in pediatric and AYA high-grade gliomas: insights from multiomic profiling.Journal of neuro-oncology · 2025Article
- The DNA Double-Strand Break Repair in Glioma: Molecular Players and Therapeutic Strategies.Molecular neurobiology · 2022Review
- Pediatric High Grade Glioma Classification Criteria and Molecular Features of a Case Series.Genes · 2022Article
- Cancer immune profiling unveils biomarkers, immunological pathways, and cell type score associated with glioblastoma patients' survival.Therapeutic advances in medical oncology · 2022Article
- Pediatric versus adult high grade glioma: Immunotherapeutic and genomic considerations.Frontiers in immunology · 2022Review
- Research highlights on contributions of mitochondrial DNA microsatellite instability in solid cancers - an overview.Contemporary oncology (Poznan, Poland) · 2022Review
- Immunohistochemical screening for mismatch repair protein deficiency in paediatric high-grade gliomas - institutional experience and review of literature.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2021Review
- Loss of SPINT2 expression frequently occurs in glioma, leading to increased growth and invasion via MMP2.Cellular oncology (Dordrecht, Netherlands) · 2020Article
- Immunotherapy for pediatric brain tumors: past and present.Neuro-oncology · 2019Review
- Characterizing temporal genomic heterogeneity in pediatric high-grade gliomas.Acta neuropathologica communications · 2017Article
- The Process and Regulatory Components of Inflammation in Brain Oncogenesis.Biomolecules · 2017Review
- Targeting the PD-1 pathway in pediatric solid tumors and brain tumors.OncoTargets and therapy · 2017Review
- Mismatch Repair Deficiency and Response to Immune Checkpoint Blockade.The oncologist · 2016Review
- Significance of glycolytic metabolism-related protein expression in colorectal cancer, lymph node and hepatic metastasis.BMC cancer · 2016Article
- Copy Number Profiling of Brazilian Astrocytomas.G3 (Bethesda, Md.) · 2016Article
- Histone turnover and chromatin accessibility: Critical mediators of neurological development, plasticity, and disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2016Article
- ATRX loss promotes tumor growth and impairs nonhomologous end joining DNA repair in glioma.Science translational medicine · 2016Article
- SPINT2 Deregulation in Prostate Carcinoma.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2016Article
Corrections and comments
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Authors and funding
10 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High grade gliomas (HGG) are one of the leading causes of cancer-related deaths in children, and there is increasing evidence that pediatric HGG may harbor distinct molecular characteristics compared to adult tumors. We have sought to clarify the role of microsatellite instability (MSI) in pediatric versus adult HGG. MSI status was determined in 144 patients (71 pediatric and 73 adults) using a well established panel of five quasimonomorphic mononucleotide repeat markers. Expression of MLH1, MSH2, MSH6 and PMS2 was determined by immunohistochemistry, MLH1 was assessed for mutations by direct sequencing and promoter methylation using MS-PCR. DNA copy number profiles were derived using array CGH, and mutations in eighteen MSI target genes studied by multiplex PCR and genotyping. MSI was found in 14/71 (19.7%) pediatric cases, significantly more than observed in adults (5/73, 6.8%; p = 0.02, Chi-square test). MLH1 expression was downregulated in 10/13 cases, however no mutations or promoter methylation were found. MSH6 was absent in one pediatric MSI-High tumor, consistent with an inherited mismatch repair deficiency associated with germline MSH6 mutation. MSI was classed as Type A, and associated with a remarkably stable genomic profile. Of the eighteen classic MSI target genes, we identified mutations only in MSH6 and DNAPKcs and described a polymorphism in MRE11 without apparent functional consequences in DNA double strand break detection and repair. This study thus provides evidence for a potential novel molecular pathway in a proportion of gliomas associated with the presence of MSI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.