An Integrated Genomic Analysis of Human Glioblastoma Multiforme
Open accessAbstract
Glioblastoma multiforme (GBM) is the most common and lethal type of brain cancer. To identify the genetic alterations in GBMs, we sequenced 20,661 protein coding genes, determined the presence of amplifications and deletions using high-density oligonucleotide arrays, and performed gene expression analyses using next-generation sequencing technologies in 22 human tumor samples. This comprehensive analysis led to the discovery of a variety of genes that were not known to be altered in GBMs. Most notably, we found recurrent mutations in the active site of isocitrate dehydrogenase 1 ( IDH1 ) in 12% of GBM patients. Mutations in IDH1 occurred in a large fraction of young patients and in most patients with secondary GBMs and were associated with an increase in overall survival. These studies demonstrate the value of unbiased genomic analyses in the characterization of human brain cancer and identify a potentially useful genetic alteration for the classification and targeted therapy of GBMs.
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IDH mutations that increase enzyme activity are early events that define major clinical and prognostic groups of gliomas.
“Gain-of-function IDH mutations are initiating events that define major clinical and prognostic classes of gliomas1,2.”
From Insulator dysfunction and oncogene activation in IDH mutant gliomas (2016) · cites this paper as [1]
The ‘High-frequency alterations of IDH1 in GBM’ section links IDH1 mutations to secondary GBM and substantially longer survival, supporting their clinical and prognostic relevance. The Discussion calls an activating effect a speculation and says further analysis is needed to determine the effect on enzyme activity. The paper does not establish that these mutations increase enzyme activity or are initiating events, and its findings concern GBM rather than gliomas broadly. (LLM, conf=0.90)
Experimental — accuracy not yet measuredGenetic and molecular markers of malignant tumors have been integrated into clinical practice, with FDA approval for several companion diagnostic devices and nucleic acid-based tests.
“Genetic and molecular markers of malignant tumors have been integrated into clinical practice 5,6 , with the US Food and Drug Administration (FDA) providing approval for several companion diagnostic devices and nucleic acid-based tests 7,8 .”
From Multimodal biomedical AI (2022) · cites this paper as [6]
The Discussion identifies IDH1 mutation as a potentially useful marker for classifying glioblastoma and says its detection is likely to be clinically useful. It does not establish that this or other markers had already been integrated into clinical practice. The FDA-approval clause has separate citations and is not attributed to this paper. (LLM, conf=0.83)
Experimental — accuracy not yet measuredPI3K signaling is hyperactivated in nearly 90% of GBMs, commonly as a consequence of EGFR amplification and activating mutation (EGFRvIII), and loss of the PTEN tumor suppressor protein.
“PI3K signaling is hyperactivated in nearly 90% of GBMs, commonly as a consequence of EGFR amplification and activating mutation (EGFRvIII), and loss of the PTEN tumor suppressor protein, a negative regulator of PI3K signaling (6–8).”
From An LXR Agonist Promotes Glioblastoma Cell Death through Inhibition of an EGFR/AKT/SREBP-1/LDLR–Dependent Pathway (2011) · cites this paper as [7]
The Integration of sequencing, copy number, and expression analyses section reports alterations in PI3K/PTEN-pathway genes in 50% of tumors and identifies EGFR and PTEN alterations in 30–40% of GBMs. It does not report PI3K signaling hyperactivation in nearly 90% of GBMs or establish EGFRvIII and PTEN protein loss as its common causes. Page numbers are unavailable in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIDH1 and IDH2 encode isocitrate dehydrogenases, and mutations in these genes are among the most frequent in diffuse gliomas.
“The IDH genes (IDH1 and IDH2) encode isocitrate dehydrogenases, and mutations in these genes are among the most frequent found in diffuse gliomas118,119.”
From Transcription factors as readers and effectors of DNA methylation (2016) · cites this paper as [118]
During DNA damage, MDM2 moves to the nucleus and regulates DNA repair independently of p53 by binding and inactivating Nbs1 within the MRE11/Rad50/NBS1 complex.
“Moreover, in the context of DNA damage, MDM2 localizes to the nucleus and modulates DNA repair in a p53-independent manner by binding to and inactivating Nbs1 in the MRE11/Rad50/NBS1 complex.1,8,27”
From Combination therapy in a xenograft model of glioblastoma: Enhancement of the antitumor activity of temozolomide by an MDM2 antagonist (2017) · cites this paper as [27]
Cancer genome sequencing efforts identified somatic mutations in IDH1 in glioblastoma multiforme in 2008.
“Cancer genome sequencing efforts yielded an unexpected discovery in 2008 with the identification of somatic mutations in a metabolic enzyme, the TCA cycle enzyme IDH1, in glioblastoma multiforme (GBM) (77).”
From Fueling Immunity: Insights into Metabolism and Lymphocyte Function (2013) · cites this paper as [77]
Genomic sequencing of gliomas and acute myelogenous leukemia identified mutations in two isoforms of NADP+-dependent isocitrate dehydrogenase (IDH1 and IDH2).
“Genomic sequencing of gliomas (Parsons et al., 2008; Yan et al., 2009) and acute myelogenous leukemia (Mardis et al., 2009) identified mutations in two isoforms of NADP+-dependent isocitrate dehydrogenase (IDH1 and IDH2).”
From Cellular Metabolism and Disease: What Do Metabolic Outliers Teach Us? (2012) · cites this paper as Parsons et al., 2008
The presence of IDH1/2 mutations in gliomas is associated with both lower histological grade and a slower rate of disease progression.
“the presence of IDH1/2 mutations in gliomas is associated with both lower histological grade and a slower rate of disease progression”
From Cellular Metabolism and Disease: What Do Metabolic Outliers Teach Us? (2012) · cites this paper as Parsons et al., 2008
D-2-HG accumulation under pathogenic conditions may contribute to tumorigenicity by stabilizing HIF-1α and impairing collagen biogenesis.
“the concentrations at which it accumulates under pathogenic conditions suggests HIF-1α stabilisation and impaired collagen biogenesis may contribute to tumorigenicity126-130.”
From Coupling Krebs cycle metabolites to signalling in immunity and cancer (2018) · cites this paper as [130]
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- [51]Contact information for the authors who directed the major components of this project is as follows: H. Yan, G. J. Riggins (clinical and sample coordination), yan00002@mc.duke.edu, griggin1@jhmi.edu; D. D. Bigner (pathological and clinical review), bigne001@mc.duke.edu; R. Karchin (bioinformatic analysis), karchin@jhu.edu; N. Papadopoulos (gene expression analysis), npapado1@jhmi.edu; G. Parmigiani (statistical analysis), gp@jhu.edu; B. Vogelstein, V. E. Velculescu, K. W. Kinzler (sequencing and copy number analysis), bertvog@gmail.com, velculescu@jhmi.edu, kinzlke@jhmi.edu. We thank N. Silliman, J. Ptak, L. Dobbyn, and M. Whalen for assistance with PCR amplification; D. Lister, L. J. Ehinger, D. L. Satterfield, J. D. Funkhouser, and P. Killela for assistance with DNA purification; T. Sjöblom for assistance with database management; the Agencourt sequencing team for assistance with automated sequencing; and C.-S. Liu and the SoftGenetics team for their assistance with mutation detection analyses. This project was carried out under the auspices of the Ludwig Brain Tumor Initiative and was supported by the Virginia and D. K. Ludwig Fund for Cancer Research, NIH grants CA121113, NS052507, CA43460, CA57345, CA62924, CA09547, 5P50-NS-20023, CA108786, and CA11898, the Pew Charitable Trusts, the Pediatric Brain Tumor Foundation Institute, the Hirschhorn Foundation, Alex’s Lemonade Stand Foundation, the American Brain Tumor Association, the American Society of Clinical Oncology, the Brain Tumor Research Fund and Beckman Coulter Corporation. Under separate licensing agreements between the Johns Hopkins University and Genzyme, Beckman Coulter, and Exact Sciences Corporations, B.V., V.E.V., and K.W.K. are entitled to a share of royalties received by the university on sales of products related to research described in this paper. These authors and the university own Genzyme and Exact Sciences stock, which is subject to certain restrictions under university policy. The terms of these arrangements are managed by the Johns Hopkins University in accordance with its conflict-of-interest policies.
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- Authors
- Parsons, D. W., Jones, S., Zhang, X., Lin, J. C.-H., Leary, R. J., Angenendt, P., Mankoo, P., Carter, H., Siu, I.-M., Gallia, G. L., Olivi, A., McLendon, R., Rasheed, B. A., Keir, S., Nikolskaya, T., Nikolsky, Y., Busam, D. A., Tekleab, H., Diaz, L. A., Hartigan, J., Smith, D. R., Strausberg, R. L., Marie, S. K. N., Shinjo, S. M. O., Yan, H., Riggins, G. J., Bigner, D. D., Karchin, R., Papadopoulos, N., Parmigiani, G., Vogelstein, B., Velculescu, V. E., & Kinzler, K. W.
- Affiliations
- Howard Hughes Medical Institute (US)
- Ludwig Center for Cancer Genetics and Therapeutics, and Howard Hughes Medical Institute at Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.
- Corresponding author
- Parsons, D. Williams
- Zhang, Xiaosong
- Lin, Jimmy Cheng-Ho
- Leary, Rebecca J.
- Angenendt, Philipp
- Vogelstein, Bert
- Velculescu, Victor E.
- Kinzler, Kenneth W.
- ORCID
- Parsons, D. Williams
- Zhang, Xiaosong
- Lin, Jimmy Cheng-Ho
- Leary, Rebecca J.
- Carter, Hannah
- Gallia, Gary L.
- Olivi, Alessandro
- McLendon, Roger
- Keir, Stephen
- Diaz, Luis A.
- Marie, Suely Kazue Nagahashi
- Yan, Hai
- Riggins, Gregory J.
- Bigner, Darell D.
- Karchin, Rachel
- Parmigiani, Giovanni
- Vogelstein, Bert
- Velculescu, Victor E.
- Kinzler, Kenneth W.
- Venue
- Science
- Published
- 2008-09-26
- Volume
- 321
- Issue
- 5897
- Pages
- 1807-1812
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC2820389
- OpenAlex
- W2040827479
- Cited by
- 5,857
- References
- 51
- Citations by year
- 2026: 131 · 2025: 160 · 2024: 189 · 2023: 260 · 2022: 256 · 2021: 370 · 2020: 344 · 2019: 313 · 2018: 329 · 2017: 347 · 2016: 353 · 2015: 373 · 2014: 410 · 2013: 428 · 2012: 457
- FWCI
- 172.43
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Scientific Electronic Library Online (São Paulo Research Foundation, Latin American and Caribbean Center on Health Sciences Information, Conselho Nacional de Desenvolvimento Científico e Tecnológico) (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health (5r01ca121113-15, 5p50ns020023-30)
- National Cancer Institute (CA108786., CA 57345, R01-CA121113, CA-121113, CA43460, CA-11898, R37CA043460, CA09547, P50CA108786, R01CA140316, P50CA062924, R37CA057345, T32CA009547, CA 62924)
- National Institute of Neurological Disorders and Stroke (5P50NS20023, R01NS052507, NS052507)
- Topics
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- glioblastoma, IDH1 mutation, IDH1, somatic mutations, gene amplification, gene deletion, gene expression profiling, secondary glioblastoma, overall survival, targeted therapy
- MeSH terms
- Adult, Brain Neoplasms, Female, Gene Amplification, Glioblastoma, Humans, Isocitrate Dehydrogenase, Male, Middle Aged, Mutation, Signal Transduction, Genome, Human, Gene Expression Regulation, Neoplastic, Survival Rate, Sequence Analysis, DNA, Gene Dosage, Mutation, Missense, Oligonucleotide Array Sequence Analysis, Polymorphism, Single Nucleotide, Gene Expression Profiling
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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