Identification of a CpG Island Methylator Phenotype that Defines a Distinct Subgroup of Glioma
Open accessAbstract
We have profiled promoter DNA methylation alterations in 272 glioblastoma tumors in the context of The Cancer Genome Atlas (TCGA). We found that a distinct subset of samples displays concerted hypermethylation at a large number of loci, indicating the existence of a glioma-CpG island methylator phenotype (G-CIMP). We validated G-CIMP in a set of non-TCGA glioblastomas and low-grade gliomas. G-CIMP tumors belong to the proneural subgroup, are more prevalent among lower-grade gliomas, display distinct copy-number alterations, and are tightly associated with IDH1 somatic mutations. Patients with G-CIMP tumors are younger at the time of diagnosis and experience significantly improved outcome. These findings identify G-CIMP as a distinct subset of human gliomas on molecular and clinical grounds.
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IDH mutant gliomas show a CpG island methylator phenotype.
“IDH mutant gliomas thus manifest a CpG island methylator phenotype (G-CIMP)10,11, though the functional significance of this altered epigenetic state remains unclear.”
From Insulator dysfunction and oncogene activation in IDH mutant gliomas (2016) · cites this paper as [10]
The Results sections report a strong association between IDH1 mutation and G-CIMP in gliomas. But in an independent set, only 35 of 48 IDH1-mutant tumors (72.9%) were G-CIMP-positive, and the paper observed no IDH2 mutations in its TCGA set. The claim is therefore broader than the paper’s finding: not all IDH1-mutant gliomas showed the phenotype, and it does not establish the association for IDH mutations generally. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIDH-mutated glioma PT2097 and IPTO2097 exhibited glioma-CpG-island methylator phenotype.
“In detail, the IDH-mutated glioma PT2097 and IPTO2097 exhibited glioma-CpG-island methylator phenotype (G-CIMP)25 (Figures 3A and 3C).”
From Individualized patient tumor organoids faithfully preserve human brain tumor ecosystems and predict patient response to therapy (2025) · cites this paper as [25]
Profiling promoters of 272 glioblastoma tumours showed that a distinct subset of samples had hypermethylation at many loci, a phenotype called CpG island methylator phenotype.
“For example, profiling the DNA methylation status in the promoters of 272 glioblastoma tumours showed that a distinct subset of samples displayed hypermethylation at a large number of loci, a phenotype termed ‘CpG island methylator phenotype’ (REF. 116).”
From Transcription factors as readers and effectors of DNA methylation (2016) · cites this paper as [116]
Interference with TET family proteins causes the CpG island methylator phenotype.
“Specifically, owing to the interference with TET family proteins, the mutation causes the CpG island methylator phenotype116,123.”
From Transcription factors as readers and effectors of DNA methylation (2016) · cites this paper as [116]
In gliomas and chondrosarcomas, IDH1 or IDH2 mutations are linked with altered DNA methylation profiles.
“in gliomas and chondrosarcomas IDH1 or IDH2 mutations have been linked with altered DNA methylation profiles (Noushmehr et al., 2010; Pansuriya et al., 2011; Turcan et al., 2012)”
From Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate (2012) · cites this paper as Noushmehr et al., 2010
iTreg cells do not require HIF-1α.
“On the other hand, induced regulatory T (iTreg) cells, also derived from naïve CD4+ T cells, do not require HIF-1α143,146.”
From Coupling Krebs cycle metabolites to signalling in immunity and cancer (2018) · cites this paper as [146]
TH17 cells rely heavily on a switch from OXPHOS to glycolysis, requiring activation of HIF-1α and induction of RORγt.
“T-helper 17 (TH17) cells, derived from naïve CD4+ T cells, are one such subset that rely heavily on a switch from OXPHOS to glycolysis, a process that requires the activation of HIF-1α and induction of RORγt143,146.”
From Coupling Krebs cycle metabolites to signalling in immunity and cancer (2018) · cites this paper as [146]
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“As another example, in disease, the GBM G-CIMP subtype is associated with IDH mutations and a characteristic methylation phenotype, while its expression profile does not define the subtype as distinctly [36].”
BackgroundBidimensional linked matrix factorization for pan-omics pan-cancer analysis
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- Authors
- Noushmehr, H., Weisenberger, D. J., Diefes, K., Phillips, H. S., Pujara, K., Berman, B. P., Pan, F., Pelloski, C. E., Sulman, E. P., Bhat, K. P., Verhaak, R. G. W., Hoadley, K. A., Hayes, D. N., Perou, C. M., Schmidt, H. K., Ding, L., Wilson, R. K., Van Den Berg, D., Shen, H., Bengtsson, H., Neuvial, P., Cope, L. M., Buckley, J., Herman, J. G., Baylin, S. B., Laird, P. W., & Aldape, K.
- Affiliations
- University of Southern California (US)
- Genentech (US)
- The University of Texas MD Anderson Cancer Center (US)
- Broad Institute (US)
- University of North Carolina at Chapel Hill (US)
- Washington University in St. Louis (US)
- University of California, Berkeley (US)
- Johns Hopkins University (US)
- Corresponding author
- Laird, Peter W.
- ORCID
- Noushmehr, Houtan
- Weisenberger, Daniel J.
- Phillips, Heidi S.
- Berman, Benjamin P.
- Pan, Fei
- Sulman, Erik P.
- Bhat, Krishna P.
- Verhaak, Roel G.W.
- Hoadley, Katherine A.
- Hayes, D. Neil
- Perou, Charles M.
- Ding, Li
- Wilson, Richard K.
- Shen, Hui
- Bengtsson, Henrik
- Neuvial, Pierre
- Cope, Leslie M.
- Buckley, Jonathan
- Herman, James G.
- Baylin, Stephen B.
- Laird, Peter W.
- Aldape, Kenneth
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2010-05
- Volume
- 17
- Issue
- 5
- Pages
- 510-522
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC2872684
- OpenAlex
- W2105528101
- Cited by
- 2,337
- References
- 67
- Citations by year
- 2026: 53 · 2025: 69 · 2024: 99 · 2023: 114 · 2022: 122 · 2021: 173 · 2020: 131 · 2019: 151 · 2018: 161 · 2017: 159 · 2016: 179 · 2015: 209 · 2014: 188 · 2013: 201 · 2012: 182
- FWCI
- 75.26
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- HAL (submittedVersion)
- Funders
- National Cancer Institute (U24CA143882, U24CA143848, U24CA126561, P50CA127001)
- Topics
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- glioma, CpG island methylator phenotype, G-CIMP, promoter methylation, glioblastoma, low-grade glioma, IDH1 mutation, copy number alterations, patient outcomes, molecular subtypes
- MeSH terms
- Brain Neoplasms, Glioblastoma, Humans, Isocitrate Dehydrogenase, Mutation, Phenotype, CpG Islands, DNA Methylation
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