ArticleBMC cancer2014
Stability of the CpG island methylator phenotype during glioma progression and identification of methylated loci in secondary glioblastomas.
Article in BMC cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Fumonisin BEpigenetics · 2025Article
- Isocitrate dehydrogenase 1 gene mutations: a case review unveiling its biological impact on disease progression, prognosis and treatment in Chilean patients.BJR case reports · 2025Review
- The Role of DNA Methylation and DNA Methyltransferases in Cancer.Advances in experimental medicine and biology · 2022Article
- FABP5 enhances malignancies of lower-grade gliomas via canonical activation of NF-κB signaling.Journal of cellular and molecular medicine · 2021Article
- Specific Glioma Prognostic Subtype Distinctions Based on DNA Methylation Patterns.Frontiers in genetics · 2019Article
- Demethylator phenotypes in acute myeloid leukemia.Leukemia · 2018Article
- Identification of an atypical etiological head and neck squamous carcinoma subtype featuring the CpG island methylator phenotype.EBioMedicine · 2017Article
- The Role of DNA Methylation in Cancer.Advances in experimental medicine and biology · 2016Review
- Biological Significance of Mutant Isocitrate Dehydrogenase 1 and 2 in Gliomagenesis.Neurologia medico-chirurgica · 2016Review
- IDH1R¹³²H decreases the proliferation of U87 glioma cells through upregulation of microRNA-128a.Molecular medicine reports · 2015Article
- DNA Methylation and Somatic Mutations Converge on the Cell Cycle and Define Similar Evolutionary Histories in Brain Tumors.Cancer cell · 2015Article
- Differential gene methylation in paired glioblastomas suggests a role of immune response pathways in tumor progression.Journal of neuro-oncology · 2015Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGrade IV glioblastomas exist in two forms, primary (de novo) glioblastomas (pGBM) that arise without precursor lesions, and the less common secondary glioblastomas (sGBM) which develop from earlier lower grade lesions. Genetic heterogeneity between pGBM and sGBM has been documented as have differences in the methylation of individual genes. A hypermethylator phenotype in grade IV GBMs is now well documented however there has been little comparison between global methylation profiles of pGBM and sGBM samples or of methylation profiles between paired early and late sGBM samples.
methodsWe performed genome-wide methylation profiling of 20 matched pairs of early and late gliomas using the Infinium HumanMethylation450 BeadChips to assess methylation at >485,000 cytosine positions within the human genome.
resultsClustering of our data demonstrated a frequent hypermethylator phenotype that associated with IDH1 mutation in sGBM tumors. In 80% of cases, the hypermethylator status was retained in both the early and late tumor of the same patient, indicating limited alterations to genome-wide methylation during progression and that the CIMP phenotype is an early event. Analysis of hypermethylated loci identified 218 genes frequently methylated across grade II, III and IV tumors indicating a possible role in sGBM tumorigenesis. Comparison of our sGBM data with TCGA pGBM data indicate that IDH1 mutated GBM samples have very similar hypermethylator phenotypes, however the methylation profiles of the majority of samples with WT IDH1 that do not demonstrate a hypermethylator phenotype cluster separately from sGBM samples, indicating underlying differences in methylation profiles. We also identified 180 genes that were methylated only in sGBM. Further analysis of these genes may lead to a better understanding of the pathology of sGBM vs pGBM.
conclusionThis is the first study to have documented genome-wide methylation changes within paired early/late astrocytic gliomas on such a large CpG probe set, revealing a number of genes that maybe relevant to secondary gliomagenesis.
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