ArticleJournal of cancer research and clinical oncology2005
Low-level microsatellite instability phenotype in sporadic glioblastoma multiforme.
Article in Journal of cancer research and clinical oncology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 40 citations in OpenAlex.
- Immune Cell Interplay in the Fight Against GBM.Cancers · 2025Review
- 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
- Incidence, clinicopathologic, and genetic characteristics of mismatch repair gene-mutated glioblastomas.Journal of neuro-oncology · 2021Article
- Current State of Immunotherapy for Treatment of Glioblastoma.Current treatment options in oncology · 2019Review
- Different behaviour of DVL1, DVL2, DVL3 in astrocytoma malignancy grades and their association to TCF1 and LEF1 upregulation.Journal of cellular and molecular medicine · 2019Article
- Classification and characterization of microsatellite instability across 18 cancer types.Nature medicine · 2016Article
- Mismatch Repair Deficiency and Response to Immune Checkpoint Blockade.The oncologist · 2016Review
- Glioblastoma multiforme therapy and mechanisms of resistance.Pharmaceuticals (Basel, Switzerland) · 2013Article
- Article
- The Changes in MGMT Promoter Methylation Status in Initial and Recurrent Glioblastomas.Translational oncology · 2012Article
- Beyond Genetics in Glioma Pathways: The Ever-Increasing Crosstalk between Epigenomic and Genomic Events.Journal of signal transduction · 2012Article
- Microsatellite instability in pediatric high grade glioma is associated with genomic profile and differential target gene inactivation.PloS one · 2011Article
- Analysis of microsatellite instability in medulloblastoma.Neuro-oncology · 2009Article
- Mismatch repair deficiency does not mediate clinical resistance to temozolomide in malignant glioma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2008Article
- Frequent loss of heterozygosity encompassing the hMLH1 locus in low grade astrocytic tumors.Journal of neuro-oncology · 2007Article
- Some speculation on the origin of glioblastoma.Neurosurgical review · 2007Review
- Article
- Alterations of p53, BCL-2, and hMSH2 protein expression in the normal brain tissues, gliosis, and gliomas.International journal of experimental pathology · 2006Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeGenetic instability is a hallmark of glioblastoma multiforme (GBM). Microsatellite instability (MSI) is a significant event in the tumorigenesis of many sporadic malignancies. The aim of our investigation was to study microsatellite instability in newly diagnosed glioblastomas.
methodsMSI was investigated in 109 GBMs with 15 microsatellite markers. Immunohistochemistry was performed for the mismatch repair (MMR) proteins hMLH1, hMSH2, hPMS2, and hMSH6 in cases showing MSI. Sequence and promoter methylation status of hMLH1 were analyzed in the case of a decreased hMLH1 protein expression as well. To further investigate MSI(+) GBMs we carried out studies of LOH at selected chromosome regions, EGFR amplification, and sequence of p53 and PTEN.
resultsMSI was observed in six GBMs (5.5%) and it was more frequent in GBMs with a previous lower grade astrocytoma (18.8% vs. 3.2%). MMR protein staining was positive in all MSI(+) GBMs except in one case, which showed an aberrant expression of hMLH1 and hPMS2 without hMLH1 inactivation. Among MSI(+) GBMs, one tumor corresponded to the GBM molecular type 1 (p53 mutation, no EGFR amplification), another tumor to type 2 (wild-type p53, EGFR amplification), and four tumors to neither type (wild-type p53, no EGFR amplification). None of the six tumors carried a PTEN mutation.
conclusionsMSI in GBM might be caused by inactivation of minor MMR genes rather than by a deficiency of hMLH1 or hMSH2 and it appears not to play a decisive role in the pathogenesis of these tumors. MSI(+) GBMs predominantly showed a profile which included wild-type of p53 and PTEN and absence of EGFR amplification but MSI occurred in all GBM molecular subtypes.
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