Integrated Genomic Analysis Identifies Clinically Relevant Subtypes of Glioblastoma Characterized by Abnormalities in PDGFRA, IDH1, EGFR, and NF1
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The Cancer Genome Atlas Network recently cataloged recurrent genomic abnormalities in glioblastoma multiforme (GBM). We describe a robust gene expression-based molecular classification of GBM into Proneural, Neural, Classical, and Mesenchymal subtypes and integrate multidimensional genomic data to establish patterns of somatic mutations and DNA copy number. Aberrations and gene expression of EGFR, NF1, and PDGFRA/IDH1 each define the Classical, Mesenchymal, and Proneural subtypes, respectively. Gene signatures of normal brain cell types show a strong relationship between subtypes and different neural lineages. Additionally, response to aggressive therapy differs by subtype, with the greatest benefit in the Classical subtype and no benefit in the Proneural subtype. We provide a framework that unifies transcriptomic and genomic dimensions for GBM molecular stratification with important implications for future studies.
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PDGFRA amplification and gain-of-function mutations are rare in IDH mutant tumors.
“Although PDGFRA is a frequent target of genomic amplification and gain-of-function mutations in glioblastoma (15%), such alterations are rare in IDH mutant tumors23,24.”
From Insulator dysfunction and oncogene activation in IDH mutant gliomas (2016) · cites this paper as [24]
The Results (Functional Annotation of Subtypes; page not available) say that most IDH1-mutant samples did not have a PDGFRA abnormality, supporting limited overlap in the glioblastomas studied. They do not establish that these alterations are rare across IDH-mutant tumors generally, or identify the observed PDGFRA mutations as gain-of-function. (LLM, conf=0.84)
Experimental — accuracy not yet measuredPDGFRA is frequently amplified or mutated in glioblastoma, at about 15%.
“Although PDGFRA is a frequent target of genomic amplification and gain-of-function mutations in glioblastoma (15%), such alterations are rare in IDH mutant tumors23,24.”
From Insulator dysfunction and oncogene activation in IDH mutant gliomas (2016) · cites this paper as [24]
The Results (Functional Annotation of Subtypes; page unavailable) report PDGFRA amplification across glioblastoma subtypes and PDGFRA mutations in some Proneural tumors. They do not give an approximately 15% frequency or establish that the mutations are gain-of-function; the authors say the point mutations may disrupt ligand interaction. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIDH mutant gliomas share the proneural transcriptional program characteristic of PDGFRA-amplified tumors.
“Nonetheless, IDH mutant gliomas strongly express PDGFRA (Fig. 2b), and share the proneural transcriptional program characteristic of PDGFRA-amplified tumors23,24.”
From Insulator dysfunction and oncogene activation in IDH mutant gliomas (2016) · cites this paper as [24]
In Results > Functional Annotation of Subtypes (page unavailable), the paper reports that 11 of 12 IDH1 mutations occurred in the Proneural class, which was also enriched for PDGFRA amplification and had a proneural expression signature. This supports the shared-program claim for the glioblastomas studied, but not its extension to IDH-mutant gliomas generally. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe prevalence of p53 mutations differs among glioblastoma molecular subtypes: proneural 54%, mesenchymal 32%, neural 21%, and classical 0%.
“The prevalence of p53 mutations differs in the different GBM molecular subtypes (proneural, mesenchymal, neural and classical) (54%, 32%, 21% and 0%, respectively) [15].”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [15]
The Results (Functional Annotation of Subtypes; page unavailable) report that TP53 mutations were frequent in Proneural samples and absent from the sequenced Classical samples, supporting a subtype difference. Our copy does not give the claimed mutation prevalences of 54%, 32%, 21%, and 0% across all four subtypes; its 54% figure refers instead to a chromosome 7/10 event in Proneural samples. (LLM, conf=0.85)
Experimental — accuracy not yet measuredUpregulation of PDGFRA is a hallmark of the proneural glioblastoma subtype.
“For example, upregulation of PDGFRA, platelet-derived growth factor receptor alpha, is a hallmark of the proneural subtype [15].”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [15]
Glioblastoma is the most common malignant primary brain tumor, but it is classified as a rare disease because its incidence rate of 3 per 100,000 people is below the rare disease definition rate of less than 10 per 100,000 people.
“While glioblastoma is the most common malignant primary brain tumor26–28, it is still classified as a “rare” disease, as its incidence rate (i.e., 3/100,000 people) is substantially lower than the rare disease definition rate (i.e., <10/100,000 people)24.”
From Federated learning enables big data for rare cancer boundary detection (2022) · cites this paper as [27]
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Self-citation
- Authors
- Verhaak, R. G. W., Hoadley, K. A., Purdom, E., Wang, V., Qi, Y., Wilkerson, M. D., Miller, C. R., Ding, L., Golub, T., Mesirov, J. P., Alexe, G., Lawrence, M., O'Kelly, M., Tamayo, P., Weir, B. A., Gabriel, S., Winckler, W., Gupta, S., Jakkula, L., Feiler, H. S., Hodgson, J. G., James, C. D., Sarkaria, J. N., Brennan, C., Kahn, A., Spellman, P. T., Wilson, R. K., Speed, T. P., Gray, J. W., Meyerson, M., Getz, G., Perou, C. M., & Hayes, D. N.
- Affiliations
- Broad Institute (US)
- University of North Carolina at Chapel Hill (US)
- University of California, Berkeley (US)
- Washington University in St. Louis (US)
- Lawrence Berkeley National Laboratory (US)
- University of California, San Francisco (US)
- Mayo Clinic (US)
- Memorial Sloan Kettering Cancer Center (US)
- SRA International (United States) (US)
- Walter and Eliza Hall Institute of Medical Research (AU)
- Corresponding author
- Hayes, D. Neil
- ORCID
- Verhaak, Roel G.W.
- Hoadley, Katherine A.
- Purdom, Elizabeth
- Wang, Victoria
- Qi, Yuan
- Wilkerson, Matthew D.
- Miller, C. Ryan
- Ding, Li
- Golub, Todd
- Mesirov, Jill P.
- Lawrence, Michael
- Tamayo, Pablo
- Gabriel, Stacey
- Winckler, Wendy
- Gupta, Supriya
- Feiler, Heidi S.
- Hodgson, J. Graeme
- James, C. David
- Sarkaria, Jann N.
- Brennan, Cameron
- Spellman, Paul T.
- Wilson, Richard K.
- Speed, Terence P.
- Gray, Joe W.
- Meyerson, Matthew
- Getz, Gad
- Perou, Charles M.
- Hayes, D. Neil
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2010-01
- Volume
- 17
- Issue
- 1
- Pages
- 98-110
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC2818769
- OpenAlex
- W2161289668
- Cited by
- 7,575
- References
- 52
- Citations by year
- 2026: 312 · 2025: 399 · 2024: 451 · 2023: 551 · 2022: 523 · 2021: 697 · 2020: 593 · 2019: 493 · 2018: 482 · 2017: 522 · 2016: 502 · 2015: 455 · 2014: 459 · 2013: 406 · 2012: 379
- FWCI
- 159.92
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion, public-domain)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Energy
- National Human Genome Research Institute (U54HG003067, U54HG003079, U54HG003273)
- National Cancer Institute (CA097257, L30 CA104183, U24CA126554, R01CA127716, CA108961, U24CA126546, U24CA126543, U24CA126563, U24CA126544, U24CA143867, U24CA143848, P50CA108961, U24CA126551, CA127716, P50 CA 58223, U24CA126561, P50CA058223, P50CA097257)
- National Institute of Neurological Disorders and Stroke (R01NS049720, NS49720)
- National Institute of Environmental Health Sciences (F30ES019449)
- National Center for Research Resources (RR023248, K12RR023248, UL1RR024992)
- Topics
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- glioblastoma, molecular subtypes, proneural subtype, mesenchymal subtype, classical subtype, PDGFRA, IDH1, EGFR, neurofibromatosis type 1, somatic mutations, gene expression signatures, neural lineage, treatment response, molecular stratification
- MeSH terms
- Adult, Aged, Brain Neoplasms, DNA Mutational Analysis, Factor Analysis, Statistical, Glioblastoma, Humans, Isocitrate Dehydrogenase, Middle Aged, Mutation, Neurofibromatosis 1, Prognosis, Gene Expression, Gene Dosage, Oligonucleotide Array Sequence Analysis, Receptor, Platelet-Derived Growth Factor alpha, Gene Expression Profiling, ErbB Receptors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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