The Somatic Genomic Landscape of Glioblastoma
Open accessAbstract
We describe the landscape of somatic genomic alterations based on multidimensional and comprehensive characterization of more than 500 glioblastoma tumors (GBMs). We identify several novel mutated genes as well as complex rearrangements of signature receptors, including EGFR and PDGFRA. TERT promoter mutations are shown to correlate with elevated mRNA expression, supporting a role in telomerase reactivation. Correlative analyses confirm that the survival advantage of the proneural subtype is conferred by the G-CIMP phenotype, and MGMT DNA methylation may be a predictive biomarker for treatment response only in classical subtype GBM. Integrative analysis of genomic and proteomic profiles challenges the notion of therapeutic inhibition of a pathway as an alternative to inhibition of the target itself. These data will facilitate the discovery of therapeutic and diagnostic target candidates, the validation of research and clinical observations and the generation of unanticipated hypotheses that can advance our molecular understanding of this lethal cancer.
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IDH 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 [23]
In Results, under “Molecular subclasses defined by global mRNA expression and DNA Methylation” (page unavailable), the paper describes G-CIMP and non-G-CIMP proneural glioblastomas as transcriptomically similar and associates PDGFRA amplification with the non-G-CIMP proneural subgroup. It reports that all IDH1-mutant cases had the G-CIMP pattern. These findings support the shared proneural program in the glioblastomas studied, but do not establish it for IDH-mutant gliomas more broadly. (LLM, conf=0.82)
Experimental — accuracy not yet measuredPDGFRA 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 [23]
The Results section on molecular subclasses associates PDGFRA amplification with the non-G-CIMP+ proneural subgroup and describes concurrent amplification in a group predominantly lacking IDH1 mutations. The Results section on somatic alterations also finds IDH1 mutations more prevalent in GBM without RTK alterations. These findings support the direction of the amplification claim in GBM, but the cited passages do not establish that PDGFRA gain-of-function mutations are rare in IDH-mutant tumors. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe promise of precision oncology has yet to be realized in GBM despite identification of relevant molecular targets.
“The promise of precision oncology has yet to be realized in GBM despite identification of relevant molecular targets (34).”
From Preclinical Modeling of Navtemadlin Pharmacokinetics, Pharmacodynamics, and Efficacy in IDH–Wild-type Glioblastoma (2025) · cites this paper as [34]
The Introduction identifies biologically relevant GBM pathways and says that functional redundancy permits adaptation to targeted molecular treatments. It describes effective therapies as a future goal, but does not directly assess whether precision oncology’s promise has been realized in GBM. (LLM, conf=0.82)
Experimental — accuracy not yet measuredDeregulation of the core p53 pathway occurs in 43% of GBM cases.
“Deregulation of the core p53 pathway occurs in 43% of cases due to: (i) TP53 gene mutation or homozygous deletion in 27.9% of cases, (ii) focal MDM2 amplification in 8–9% of cases, and (iii) focal MDM4 amplification in 7–9% of cases.”
From Preclinical Efficacy of the MDM2 Inhibitor RG7112 in <i>MDM2</i> -Amplified and <i>TP53</i> Wild-type Glioblastomas (2016) · cites this paper as [4]
In Results, ‘The landscape of somatic alterations in glioblastoma’ (page unavailable), the paper reports TP53 mutation/deletion in 27.9% of tumors and MDM1/2/4 amplification in 15.1%. Those figures total approximately 43%, but the paper reports 85.3% dysregulation of the p53 pathway when CDKN2A deletion is included. It does not give the cited separate 8–9% amplification rates for MDM2 and MDM4. (LLM, conf=0.84)
Experimental — accuracy not yet measuredTP53 gene mutation or homozygous deletion occurs in 27.9% of GBM cases.
“Deregulation of the core p53 pathway occurs in 43% of cases due to: (i) TP53 gene mutation or homozygous deletion in 27.9% of cases, (ii) focal MDM2 amplification in 8–9% of cases, and (iii) focal MDM4 amplification in 7–9% of cases.”
From Preclinical Efficacy of the MDM2 Inhibitor RG7112 in <i>MDM2</i> -Amplified and <i>TP53</i> Wild-type Glioblastomas (2016) · cites this paper as [4]
In Results, ‘The landscape of somatic alterations in glioblastoma’ (page not provided), the paper reports TP53 mutation or deletion in 27.9% of tumors. It does not specify that the deletions counted in that figure were homozygous, so the claim’s narrower deletion type is not established by our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measured
The vast majority of GBM exhibits disruption of three major signaling pathways: tyrosine kinase receptor, retinoblastoma, and p53.
“The TCGA has demonstrated that the vast majority of GBM exhibits, through various genetic mechanisms, disruption of three major signaling pathways [4]: (i) tyrosine kinase receptor pathway, (ii) retinoblastoma pathway and (iii) p53 pathway.”
From Preclinical Efficacy of the MDM2 Inhibitor RG7112 in <i>MDM2</i> -Amplified and <i>TP53</i> Wild-type Glioblastomas (2016) · cites this paper as [4]
The Results section (“The landscape of somatic alterations in glioblastoma”; page not provided) reports alterations affecting the p53 pathway in 85.3% of tumors and Rb function in 78.9%, supporting widespread disruption of those pathways. It reports an altered receptor tyrosine kinase (RTK) in 67.3%, but does not show that the vast majority of tumors had disruption of all three pathways. (LLM, conf=0.86)
Experimental — accuracy not yet measuredFocal MDM4 amplification occurs in 7-9% of GBM cases.
“Deregulation of the core p53 pathway occurs in 43% of cases due to: (i) TP53 gene mutation or homozygous deletion in 27.9% of cases, (ii) focal MDM2 amplification in 8–9% of cases, and (iii) focal MDM4 amplification in 7–9% of cases.”
From Preclinical Efficacy of the MDM2 Inhibitor RG7112 in <i>MDM2</i> -Amplified and <i>TP53</i> Wild-type Glioblastomas (2016) · cites this paper as [4]
The Results section (‘The landscape of somatic alterations in glioblastoma’; page unavailable) includes MDM4 among amplified MDM-family genes in GBM. It reports 15.1% for MDM1/2/4 combined, however, not a separate 7–9% frequency for focal MDM4 amplification. (LLM, conf=0.84)
Experimental — accuracy not yet measuredFocal MDM2 amplification occurs in 8-9% of GBM cases.
“Deregulation of the core p53 pathway occurs in 43% of cases due to: (i) TP53 gene mutation or homozygous deletion in 27.9% of cases, (ii) focal MDM2 amplification in 8–9% of cases, and (iii) focal MDM4 amplification in 7–9% of cases.”
From Preclinical Efficacy of the MDM2 Inhibitor RG7112 in <i>MDM2</i> -Amplified and <i>TP53</i> Wild-type Glioblastomas (2016) · cites this paper as [4]
The Results sections on genomic gains and losses and on somatic alterations report MDM2 amplification in GBM. However, the only percentage given is 15.1% for amplification of MDM1, MDM2, or MDM4 combined; our copy does not give an 8–9% frequency for focal MDM2 amplification alone. (LLM, conf=0.87)
Experimental — accuracy not yet measuredThe majority of GBM tumors harbor molecular alterations that affect normal p53 function, including TP53 mutation (22%), amplification of MDM2 (10%) or MDM4 (9%), and/or CDKN2A/B homozygous deletion (60%).
“These alterations include TP53 mutation (22%), amplification of MDM2 (10%) or MDM4 (9%), and/or CDKN2A/B homozygous deletion (60%).4,5”
From Pharmacokinetic-pharmacodynamic-efficacy modeling of the MDM2 inhibitor brigimadlin in glioblastoma patient-derived xenografts (2026) · cites this paper as [5]
The Results section ('The landscape of somatic alterations in glioblastoma'; page unavailable) reports p53-pathway dysregulation in 85.3% of tumors, supporting the claim that a majority have relevant alterations. Its figures do not establish the cited breakdown: it reports TP53 mutation/deletion at 27.9%, combined MDM1/2/4 amplification at 15.1%, and CDKN2A deletion at 57.8%, rather than the stated individual percentages and alteration types. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe TP53 gene was mutated in approximately 28% of glioblastoma tumors, with lower grade gliomas exhibiting more than 90% TP53 mutations in co-occurrence with IDH1 mutations.
“Upon closer analysis, the TP53 gene was mutated in ~28% of tumors with lower grade gliomas exhibiting >90% TP53 mutations in co-occurrence with IDH1 mutations [14].”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [14]
In Results, ‘The landscape of somatic alterations in glioblastoma’ (page unavailable), the paper reports TP53 mutation or deletion in 27.9% of GBMs, close to the claimed 28% but not limited to mutations. It also reports concurrent TP53 mutations in 12 of 13 IDH1-mutant GBMs and notes a similar pattern in lower-grade gliomas; it does not give a >90% figure for lower-grade gliomas. (LLM, conf=0.88)
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 [23]
The p53 pathway, including CDKN2A, MDM2 and TP53, was deregulated in approximately 85% of tumors in The Cancer Genome Atlas glioblastoma project.
“The latest iteration of The Cancer Genome Atlas (TCGA) GBM project shows that the p53 pathway (including CDKN2A, MDM2 and TP53) was deregulated in ~85% of tumors [14].”
From The p53 Pathway in Glioblastoma (2018) · cites this paper as [14]
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 [26]
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BackgroundSelf-citationSumazin, P., Yang, X., Chiu, H., Chung, W., Iyer, A. P., Llobet‐Navàs, D., Rajbhandari, P., Bansal, M., Guarnieri, P., Silva, J., et al. (2011) · Cell · doi:10.1016/j.cell.2011.09.041 · Cited by 692 · cited 2× · see citing works
“ceRNAs are mRNAs coregulated in trans by a common miR (Sumazin et al., 2011; Tay et al., 2011).”
BackgroundFisher, S., Barry, A. J., Abreu, J., Minie, B., Nolan, J., Delorey, T. M., Young, G., Fennell, T. J., Allen, A., Ambrogio, L., et al. (2011) · Genome biology · doi:10.1186/gb-2011-12-1-r1 · Cited by 683 · see citing works
Self-citationMutual exclusivity analysis identifies oncogenic network modulesPreprint
Ciriello, G., Cerami, E. G., Sander, C., & Schultz, N. D. (2011) · Genome Research · doi:10.1101/gr.125567.111 · Cited by 676 · cited 2× · see citing works
“Unsupervised analysis of 251 GBMs with both copy number and WES mutation data identified genes sets (modules) in which somatic alterations were significantly mutually exclusive (MEMo; Ciriello et al., 2012).”
BackgroundMethodSelf-citationLovejoy, C. A., Li, W., Reisenweber, S., Thongthip, S., Bruno, J., de Lange, T., De, S., Petrini, J. H. J., Sung, P. A., Jasin, M., et al. (2012) · PLoS Genetics · doi:10.1371/journal.pgen.1002772 · Cited by 629 · see citing works
miR-29 miRNAs activate p53 by targeting p85α and CDC42
Park, S. Y., Lee, J. H., Ha, M., Nam, J., & Kim, V. N. (2008) · Nature Structural & Molecular Biology · doi:10.1038/nsmb.1533 · Cited by 608 · see citing works
IDH1 mutations are present in the majority of common adult gliomas but rare in primary glioblastomas
Ichimura, K., Pearson, D. M., Kocialkowski, S., Bäcklund, L. M., Chan, R., Jones, D., & Collins, V. P. (2009) · Neuro-Oncology · doi:10.1215/15228517-2009-025 · Cited by 593 · see citing works
Emerging insights into the molecular and cellular basis of glioblastomaPreprint
Dunn, G. P., Rinne, M. L., Wykosky, J., Genovese, G., Quayle, S. N., Dunn, I. F., Agarwalla, P. K., Chheda, M. G., Campos, B., Wang, A., et al. (2012) · Genes & Development · doi:10.1101/gad.187922.112 · Cited by 559 · cited 1× · see citing works
“Although reported median survival for patients with GBM ranges from 12–18 months, a subset of individuals will survive for more than 3 years (Dolecek et al., 2012; Dunn et al., 2012).”
BackgroundSelf-citationInda, M.-D.-M., Bonavia, R., Mukasa, A., Narita, Y., Sah, D. W. Y., VandenBerg, S. R., Brennan, C. W., Johns, T. G., Bachoo, R. M., Hadwiger, P., et al. (2010) · Genes & Development · doi:10.1101/gad.1890510 · Cited by 543 · see citing works
Self-citationSzerlip, N. J., Pedraza, A. M., Chakravarty, D., Azim, M., McGuire, J., Fang, Y., Ozawa, T., Holland, E. C., Huse, J. T., Jhanwar, S. C., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1114033109 · Cited by 538 · cited 1× · see citing works
“4%, 14/33), as did the majority of MET-altered tumors (3/4), reflecting a pattern of intratumoral heterogeneity that has been previously documented by in situ hybridization (Snuderl et al., 2011; Szerlip et al., 2012).”
BackgroundSelf-citationBrennan, C. W., Momota, H., Hambardzumyan, D., Ozawa, T., Tandon, A., Pedraza, A. M., & Holland, E. C. (2009) · PLoS ONE · doi:10.1371/journal.pone.0007752 · Cited by 534 · cited 1× · see citing works
“Notch1 and Notch3 expression were moderately increased in classical tumors, consistent with previous reports linking EGFR and Notch activation in GBM (Brennan et al., 2009).”
ResultSelf-citationYan, H., Killela, P. J., Reitman, Z. J., Jiao, Y., Bettegowda, C., Agrawal, N., Diaz, L. A., Friedman, A. H., Friedman, H. S., Gallia, G. L., et al. (2014) · Neuro-Oncology · doi:10.1093/neuonc/nou206.18 · Cited by 530 · see citing works
Self-citationCostello, M., Pugh, T. J., Fennell, T. J., Stewart, C., Lichtenstein, L., Meldrim, J. C., Fostel, J., Friedrich, D. C., Perrin, D., Dionne, D. A., et al. (2013) · Nucleic Acids Research · doi:10.1093/nar/gks1443 · Cited by 523 · see citing works
Self-citationLiu, X.-Y., Gerges, N., Korshunov, A., Sabha, N., Khuong-Quang, D.-A., Fontebasso, A. M., Fleming, A. J., Hadjadj, D., Schwartzentruber, J., Majewski, J., et al. (2012) · Acta Neuropathologica · doi:10.1007/s00401-012-1031-3 · Cited by 428 · cited 2× · see citing works
“These included spectrin alpha 1 (SPTA1, mutated in 9%), which encodes a cell motility protein that interacts with the ABL oncogene and is related to various hereditary red blood cell disorders; ATRX (6%), a member of the SWI/SNF family of chromatin remodelers recently implicated in pediatric and adult high-grade gliom…”
BackgroundNatural selection on human microRNA binding sites inferred from SNP data
Chen, K., & Rajewsky, N. (2006) · Nature Genetics · doi:10.1038/ng1910 · Cited by 391 · see citing works
Self-citationBady, P., Sciuscio, D., Diserens, A., Bloch, J., van den Bent, M. J., Marosi, C., Dietrich, P.-Y., Weller, M., Mariani, L., Heppner, F. L., et al. (2012) · Acta Neuropathologica · doi:10.1007/s00401-012-1016-2 · Cited by 345 · see citing works
Vivanco, I., Robins, H. I., Rohle, D., Campos, C., Grommes, C., Nghiemphu, P. L., Kubek, S., Oldrini, B., Chheda, M. G., Yannuzzi, N. A., et al. (2012) · Cancer Discovery · doi:10.1158/2159-8290.cd-11-0284 · Cited by 343 · cited 1× · see citing works
“While the development of a therapeutic strategy targeting mutated EGFR could have a major impact on survival and continues to be a topic of great interest (Vivanco et al., 2012), strategies will need to address the possibility that different EGFR alterations might exist concurrently in a tumor and yield differential b…”
BackgroundSelf-citationGenomic sequencing of colorectal adenocarcinomas identifies a recurrent VTI1A-TCF7L2 fusion
Bass, A. J., Lawrence, M. S., Brace, L. E., Ramos, A. H., Drier, Y., Cibulskis, K., Sougnez, C. L., Voet, D., Saksena, G., Sivachenko, A., et al. (2011) · Nature Genetics · doi:10.1038/ng.936 · Cited by 309 · see citing works
Self-citationCyclooxygenase-2 expression in human gliomas: prognostic significance and molecular correlations.
Shono, T., Tofilon, P. J., Bruner, J. M., Owolabi, O., & Lang, F. F. (2001) · PubMed · Cited by 302 · see citing works
Whole exome sequencing identifies ATRX mutation as a key molecular determinant in lower-grade glioma
Kannan, K. S., Inagaki, A., Silber, J., Gorovets, D. J., Zhang, J., Kastenhuber, E. R., Heguy, A., Petrini, J. H. J., Chan, T. A.-T., & Huse, J. T. (2012) · Oncotarget · doi:10.18632/oncotarget.689 · Cited by 277 · cited 1× · see citing works
“These included spectrin alpha 1 (SPTA1, mutated in 9%), which encodes a cell motility protein that interacts with the ABL oncogene and is related to various hereditary red blood cell disorders; ATRX (6%), a member of the SWI/SNF family of chromatin remodelers recently implicated in pediatric and adult high-grade gliom…”
BackgroundSelf-citationPDGFRA gene rearrangements are frequent genetic events in PDGFRA-amplified glioblastomasPreprint
Ozawa, T., Brennan, C. W., Wang, L., Squatrito, M., Sasayama, T., Nakada, M., Huse, J. T., Pedraza, A. M., Utsuki, S., Yasui, Y., et al. (2010) · Genes & Development · doi:10.1101/gad.1972310 · Cited by 216 · cited 1× · see citing works
“This result is concordant with previously reported estimates of D8,9 expression (Ozawa et al., 2010).”
ResultSelf-citationBengtsson, H. L., Simpson, K., Bullard, J. W., & Hansen, K. D. (2008) · UC Berkeley · Cited by 149 · see citing works
Comment on "The Consensus Coding Sequences of Human Breast and Colorectal Cancers"
Getz, G. A., Höfling, H., Mesirov, J. P., Golub, T. R., Meyerson, M. M., Tibshirani, R. J., & Lander, E. S. (2007) · Science · doi:10.1126/science.1138764 · Cited by 130 · see citing works
Self-citationIntegrated genomic analyses of ovarian carcinoma
The Cancer Genome Atlas Research Network (2011) · Nature · doi:10.1038/nature10166 · Cited by 129 · see citing works
Feedback Circuit among INK4 Tumor Suppressors Constrains Human Glioblastoma Development
Wiedemeyer, R., Brennan, C. W., Heffernan, T. P., Xiao, Y., Mahoney, J. E., Protopopov, A. I., Zheng, H., Bignell, G. R., Furnari, F. B., Cavenee, W. K., et al. (2008) · Cancer Cell · doi:10.1016/j.ccr.2008.02.010 · Cited by 119 · see citing works
Self-citationHolmes, K. M., Annala, M., Chua, C. Y. X., Dunlap, S. M., Liu, Y., Hugen, N., Moore, L. M., Cogdell, D. E., Hu, L., Nykter, M., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1120375109 · Cited by 118 · see citing works
Self-citationSanborn, Z., Salama, S. R., Grifford, M., Brennan, C. W., Mikkelsen, T., Jhanwar, S. C., Katzman, S. J., Chin, L., & Haussler, D. H. (2013) · Cancer Research · doi:10.1158/0008-5472.can-13-0186 · Cited by 111 · cited 5× · see citing works
“Among tumors expressing D12–13mRNA, analysis of aberrant junctions in WGS data (BamBam) failed to identify concordant DNA deletion in 14/15 cases where data were available.”
BackgroundMethodInfluentialSelf-citationSTAR RNA-binding protein Quaking suppresses cancer via stabilization of specific miRNAPreprint
Chen, A.-J., Paik, J.-H., Zhang, H., Shukla, S. A., Mortensen, R., HU, J. L., Ying, H., Hu, B., Hurt, J. A., Farny, N. G., et al. (2012) · Genes & Development · doi:10.1101/gad.189001.112 · Cited by 111 · cited 1× · see citing works
“This is consistent with a recent publication demonstrating thatQKI functions as a tumor suppressor in GBM by acting as a p53-responsive regulator of mature miR-20a stability to regulate TGFbR2 expression and TGFb network signaling (Chen et al., 2012).”
BackgroundSelf-citationKuttler, F., & Mai, S. (2006) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2006.10.007 · Cited by 83 · cited 1× · see citing works
“These reconstructed circles are most consistent with extrachromosomal double minute chromosomes (Kuttler and Mai, 2007).”
BackgroundDNA hypermethylation profiles associated with glioma subtypes and EZH2 and IGFBP2 mRNA expression
Zheng, S., Houseman, E. A., Morrison, Z. D., Wrensch, M., Patoka, J. S., Ramos, C., Haas-Kogan, D. A., McBride, S. M., Marsit, C. J., Christensen, B. C., et al. (2011) · Neuro-Oncology · doi:10.1093/neuonc/noq190 · Cited by 75 · cited 1× · see citing works
“, 2001), and low IGFBP2 expression has been associated with global DNA hypermethylation in glioma (Zheng et al., 2011).”
BackgroundSelf-citationZheng, S., Fu, J., Vegesna, R., Mao, Y., Heathcock, L. E., Torres‐García, W., Ezhilarasan, R., Wang, S., McKenna, A., Chin, L., et al. (2013) · Genes & Development · doi:10.1101/gad.213686.113 · Cited by 73 · cited 2× · see citing works
“A high frequency of structural variants on the q arm of chromosome 12, involving the MDM2 and CDK4 genes, was observed and associated with the presence of double minute, extrachromosomal DNA fragments, which may be functionally relevant (Zheng et al., 2013).”
BackgroundMethodSelf-citationCho, J., Pastorino, S., Zeng, Q., Xu, X., Johnson, W. E., VandenBerg, S. R., Verhaak, R. G. W., Cherniack, A. D., Watanabe, H., Dutt, A., et al. (2011) · Cancer Research · doi:10.1158/0008-5472.can-11-0821 · Cited by 73 · cited 1× · see citing works
“C-terminal deletion variants have previously been associated with gliomagenesis in experimental rodent systems in vivo (Cho et al., 2011).”
BackgroundSelf-citationIsolation and characterization of a novel gene deleted in DiGeorge syndrome
Kurahashi, H., Akagi, K., Inazawa, J., Ohta, T., Niikawa, N., Kayatani, F., Sano, T., Okada, S., & Nishisho, I. (1995) · Human Molecular Genetics · doi:10.1093/hmg/4.4.541 · Cited by 72 · cited 1× · see citing works
“LZTR1, a putative transcriptional regulator associated with the DiGeorge congenital developmental syndrome (Kurahashi et al., 1995), has not previously been implicated in cancer.”
BackgroundCallaghan, T., Antczak, M., Flickinger, T. W., Raines, M. A., Myers, M., & Kung, H. J. (1993) · PubMed · Cited by 39 · see citing works
Schittenhelm, J., Trautmann, K., Tabatabai, G., Hermann, C., Meyermann, R., & Beschorner, R. (2009) · Modern Pathology · doi:10.1038/modpathol.2009.132 · Cited by 28 · cited 1× · see citing works
“Members of the annexin family have been associated with glioma growth and migration, and annexin-1 is known to be underexpressed in secondary but not primary GBM (Schittenhelm et al., 2009).”
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Single-cell RNA-seq highlights intratumoral heterogeneity in primary glioblastoma
Patel, A. P., Tirosh, I., Trombetta, J. J., Shalek, A. K., Gillespie, S. M., Wakimoto, H., Cahill, D. P., Nahed, B. V., Curry, W. T., Martuza, R. L., et al. (2014) · Science · doi:10.1126/science.1254257 · Cited by 5,063 · see citing works
TCGAbiolinks: an R/Bioconductor package for integrative analysis of TCGA data
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Self-citationReview The Cancer Genome Atlas (TCGA): an immeasurable source of knowledge
Tomczak, K. J., Czerwińska, P., & Wiznerowicz, M. (2015) · Współczesna Onkologia · doi:10.5114/wo.2014.47136 · Cited by 3,503 · see citing works
Oncogenic Signaling Pathways in The Cancer Genome Atlas
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Self-citationComprehensive, Integrative Genomic Analysis of Diffuse Lower-Grade Gliomas
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Genomic classification of cutaneous melanoma
Akbani, R., Akdemir, K. C., Aksoy, B. A., Albert, M., Ally, A., Amin, S. B., Arachchi, H., Arora, A., Auman, J. T., Ayala, B., et al. (2015) · Cell · doi:10.1016/j.cell.2015.05.044 · Cited by 3,151 · see citing works
Self-citationAn Integrative Model of Cellular States, Plasticity, and Genetics for Glioblastoma
Neftel, C., Laffy, J., Filbin, M. G., Hara, T., Shore, M. E., Rahme, G. J., Richman, A. R., Silverbush, D., Shaw, M. L., Hebert, C. M., et al. (2019) · Cell · doi:10.1016/j.cell.2019.06.024 · Cited by 2,781 · see citing works
The epidemiology of glioma in adults: a "state of the science" review
Ostrom, Q. T., Bauchet, L., Davis, F. G., Deltour, I., Fisher, J. L., Langer, C. E., Pekmezci, M., Schwartzbaum, J., Turner, M. C., Walsh, K. M., et al. (2014) · Neuro-Oncology · doi:10.1093/neuonc/nou087 · Cited by 2,229 · see citing works
Self-citationCeccarelli, M., Barthel, F. P., Malta, T. M., Sabedot, T. S., Salama, S. R., Murray, B. A., Morozova, O., Newton, Y., Radenbaugh, A., Pagnotta, S. M., et al. (2016) · Cell · doi:10.1016/j.cell.2015.12.028 · Cited by 2,200 · see citing works
Self-citationPI3K/AKT/mTOR signaling transduction pathway and targeted therapies in cancer
Glaviano, A., Foo, A. S. C., Lam, H. Y., Yap, K. C. H., Jacot, W., Jones, R. H., Eng, H., Nair, M. G., Makvandi, P., Geoerger, B., et al. (2023) · Molecular Cancer · doi:10.1186/s12943-023-01827-6 · Cited by 2,138 · see citing works
“Mutations in PI3K family genes, especially PIK3CA or PIK3R1 are often present in glioblastoma multiforme [74], testicular germ cell tumors [75], and Ewing’s sarcoma [76], resulting in alteration pattern of PAM pathway.”
BackgroundSelf-citationWang, Q., Hu, B., Hu, X., Kim, H., Squatrito, M., Scarpace, L. M., deCarvalho, A. C., Lyu, S., Li, P., Li, Y., et al. (2017) · Cancer Cell · doi:10.1016/j.ccell.2017.06.003 · Cited by 1,975 · see citing works
Self-citationGlioma Groups Based on 1p/19q, IDH , and TERT Promoter Mutations in Tumors
Eckel‐Passow, J. E., Lachance, D. H., Molinaro, A. M., Walsh, K. M., Decker, P. A., Sicotte, H., Pekmezci, M., Rice, T., Kosel, M., Smirnov, I. V., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1407279 · Cited by 1,984 · see citing works
Self-citationVemurafenib in Multiple Nonmelanoma Cancers with <i>BRAF</i> V600 Mutations
Hyman, D. M., Puzanov, I., Subbiah, V., Faris, J. E., Chau, I., Blay, J.-Y., Wolf, J., Raje, N. S., Diamond, E. L., Hollebecque, A., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1502309 · Cited by 1,764 · see citing works
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Cancer stem cells in glioblastomaPreprint
Lathia, J. D., Mack, S. C., Mulkearns-Hubert, E. E., Valentim, C. L. L., & Rich, J. N. (2015) · Genes & Development · doi:10.1101/gad.261982.115 · Cited by 1,600 · see citing works
Towards a general-purpose foundation model for computational pathology
Chen, R. J., Ding, T., Lu, M. Y., Williamson, D. F. K., Jaume, G., Song, A. H., Chen, B., Zhang, A., Shao, D., Shaban, M., et al. (2024) · Nature Medicine · doi:10.1038/s41591-024-02857-3 · Cited by 1,560 · see citing works
Landscape of Microsatellite Instability Across 39 Cancer Types
Bonneville, R., Krook, M. A., Kautto, E. A., Miya, J., Wing, M. R., Chen, H., Reeser, J. W., Yu, L., & Roychowdhury, S. (2017) · JCO Precision Oncology · doi:10.1200/po.17.00073 · Cited by 1,474 · see citing works
The BioGRID interaction database: 2019 update
Oughtred, R., Stark, C., Breitkreutz, B., Rust, J., Boucher, L., Chang, C., Kolas, N. K., O’Donnell, L., Leung, G. C., McAdam, R. F., et al. (2018) · Nucleic Acids Research · doi:10.1093/nar/gky1079 · Cited by 1,440 · see citing works
Zhang, S., Zhao, B. S., Zhou, A., Lin, K., Zheng, S., Lu, Z., Chen, Y., Sulman, E. P., Xie, K., Bögler, O., et al. (2017) · Cancer Cell · doi:10.1016/j.ccell.2017.02.013 · Cited by 1,453 · see citing works
Self-citationInsulator dysfunction and oncogene activation in IDH mutant gliomas
Flavahan, W. A., Drier, Y., Liau, B. B., Gillespie, S. M., Venteicher, A. S., Stemmer-Rachamimov, A. O., Suvà, M. L., & Bernstein, B. E. (2016) · Nature · doi:10.1038/nature16490 · Cited by 1,288 · see citing works
Epidemiologic and Molecular Prognostic Review of Glioblastoma
Thakkar, J. P., Dolecek, T. A., Horbinski, C., Ostrom, Q. T., Lightner, D. D., Barnholtz‐Sloan, J. S., & Villano, J. L. (2014) · Cancer Epidemiology Biomarkers & Prevention · doi:10.1158/1055-9965.epi-14-0275 · Cited by 1,392 · see citing works
Self-citationEpigenetic Determinants of CancerPreprint
Baylin, S. B., & Jones, P. A. (2016) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a019505 · Cited by 1,363 · see citing works
Self-citationA compendium of mutational cancer driver genes
Martínez-Jiménez, F., Muiños, F., Sentís, I., Deu-Pons, J., Reyes-Salazar, I., Arnedo-Pac, C., Mularoni, L., Pich, O., Bonet, J., Kranas, H., et al. (2020) · Nature reviews. Cancer · doi:10.1038/s41568-020-0290-x · Cited by 1,278 · see citing works
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Self-citationPan-cancer whole-genome analyses of metastatic solid tumours
Priestley, P., Baber, J., Lolkema, M. P., Steeghs, N., de Bruijn, E., Shale, C., Duyvesteyn, K., Haidari, S., van Hoeck, A., Onstenk, W., et al. (2019) · Nature · doi:10.1038/s41586-019-1689-y · Cited by 1,106 · see citing works
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Self-citationGlioblastoma: Overview of Disease and Treatment
Davis, M. E. (2016) · Clinical journal of oncology nursing · doi:10.1188/16.cjon.s1.2-8 · Cited by 1,222 · see citing works
Treating cancer with selective CDK4/6 inhibitors
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Self-citationWeller, M., Butowski, N. A., Tran, D. D., Recht, L. D., Lim, M. K., Hirte, H. W., Ashby, L. S., Mechtler, L. L., Goldlust, S. A., IWAMOTO, F. M., et al. (2017) · The Lancet Oncology · doi:10.1016/s1470-2045(17)30517-x · Cited by 1,138 · see citing works
Self-citationWeller, M., Wick, W., Aldape, K. D., Brada, M., Berger, M. S., Pfister, S. M., Nishikawa, R., Rosenthal, M. A., Wen, P. Y., Stupp, R., et al. (2015) · Nature Reviews Disease Primers · doi:10.1038/nrdp.2015.17 · Cited by 1,129 · see citing works
Self-citationMechanisms of receptor tyrosine kinase activation in cancer
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Genomic and Functional Approaches to Understanding Cancer Aneuploidy
Taylor, A. M., Shih, J., Ha, G., Gao, G. F., Zhang, X., Berger, A. C., Schumacher, S. E., Wang, C., Hu, H., Liu, J., et al. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.03.007 · Cited by 1,068 · see citing works
Self-citationThe BioGRID interaction database: 2017 update
Chatr‐aryamontri, A., Oughtred, R., Boucher, L., Rust, J., Chang, C., Kolas, N. K., O’Donnell, L., Oster, S. K., Theesfeld, C. L., Sellam, A., et al. (2016) · Nucleic Acids Research · doi:10.1093/nar/gkw1102 · Cited by 960 · see citing works
Delineating copy number and clonal substructure in human tumors from single-cell transcriptomes
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Self-citationImmune and genomic correlates of response to anti-PD-1 immunotherapy in glioblastoma
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- Authors
- Brennan, C. W., Verhaak, R. G. W., McKenna, A., Campos, B., Noushmehr, H., Salama, S. R., Zheng, S., Chakravarty, D., Sanborn, J. Z., Berman, S. H., Beroukhim, R., Bernard, B., Wu, C.-J., Genovese, G., Shmulevich, I., Barnholtz-Sloan, J., Zou, L., Vegesna, R., Shukla, S. A., Ciriello, G., Yung, W. K., Zhang, W., Sougnez, C., Mikkelsen, T., Aldape, K., Bigner, D. D., Van Meir, E. G., Prados, M., Sloan, A., Black, K. L., Eschbacher, J., Finocchiaro, G., Friedman, W., Andrews, D. W., Guha, A., Iacocca, M., O’Neill, B. P., Foltz, G., Myers, J., Weisenberger, D. J., Penny, R., Kucherlapati, R., Perou, C. M., Hayes, D. N., Gibbs, R., Marra, M., Mills, G. B., Lander, E., Spellman, P., Wilson, R., Sander, C., Weinstein, J., Meyerson, M., Gabriel, S., Laird, P. W., Haussler, D., Getz, G., Chin, L., Benz, C., Barnholtz-Sloan, J., Barrett, W., Ostrom, Q., Wolinsky, Y., Black, K. L., Bose, B., Boulos, P. T., Boulos, M., Brown, J., Czerinski, C., Eppley, M., Iacocca, M., Kempista, T., Kitko, T., Koyfman, Y., Rabeno, B., Rastogi, P., Sugarman, M., Swanson, P., Yalamanchii, K., Otey, I. P., Liu, Y. S., Xiao, Y., Auman, J. T., Chen, P.-C., Hadjipanayis, A., Lee, E., Lee, S., Park, P. J., Seidman, J., Yang, L., Kucherlapati, R., Kalkanis, S., Mikkelsen, T., Poisson, L. M., Raghunathan, A., Scarpace, L., Bernard, B., Bressler, R., Eakin, A., Iype, L., Kreisberg, R. B., Leinonen, K., Reynolds, S., Rovira, H., Thorsson, V., Shmulevich, I., Annala, M. J., Penny, R., Paulauskis, J., Curley, E., Hatfield, M., Mallery, D., Morris, S., Shelton, T., Shelton, C., Sherman, M., Yena, P., Cuppini, L., DiMeco, F., Eoli, M., Finocchiaro, G., Maderna, E., Pollo, B., Saini, M., Balu, S., Hoadley, K. A., Li, L., Miller, C. R., Shi, Y., Topal, M. D., Wu, J., Dunn, G., Giannini, C., O'Neill, B. P., Aksoy, B. A., Antipin, Y., Borsu, L., Berman, S. H., Brennan, C. W., Cerami, E., Chakravarty, D., Ciriello, G., Gao, J., Gross, B., Jacobsen, A., Ladanyi, M., Lash, A., Liang, Y., Reva, B., Sander, C., Schultz, N., Shen, R., Socci, N. D., Viale, A., Ferguson, M. L., Chen, Q.-R., Demchok, J. A., Dillon, L. A. L., Shaw, K. R. M., Sheth, M., Tarnuzzer, R., Wang, Z., Yang, L., Davidsen, T., Guyer, M. S., Ozenberger, B. A., Sofia, H. J., Bergsten, J., Eckman, J., Harr, J., Myers, J., Smith, C., Tucker, K., Winemiller, C., Zach, L. A., Ljubimova, J. Y., Eley, G., Ayala, B., Jensen, M. A., Kahn, A., Pihl, T. D., Pot, D. A., Wan, Y., Eschbacher, J., Foltz, G., Hansen, N., Hothi, P., Lin, B., Shah, N., Yoon, J.-G., Lau, C., Berens, M., Ardlie, K., Beroukhim, R., Carter, S. L., Cherniack, A. D., Noble, M., Cho, J., Cibulskis, K., DiCara, D., Frazer, S., Gabriel, S. B., Gehlenborg, N., Gentry, J., Heiman, D., Kim, J., Jing, R., Lander, E. S., Lawrence, M., Lin, P., Mallard, W., Meyerson, M., Onofrio, R. C., Saksena, G., Schumacher, S., Sougnez, C., Stojanov, P., Tabak, B., Voet, D., Zhang, H., Zou, L., Getz, G., Dees, N. N., Ding, L., Fulton, L. L., Fulton, R. S., Kanchi, K.-L., Mardis, E. R., Wilson, R. K., Baylin, S. B., Andrews, D. W., Harshyne, L., Cohen, M. L., Devine, K., Sloan, A. E., VandenBerg, S. R., Berger, M. S., Prados, M., Carlin, D., Craft, B., Ellrott, K., Goldman, M., Goldstein, T., Grifford, M., Haussler, D., Ma, S., Ng, S., Salama, S. R., Sanborn, J. Z., Stuart, J., Swatloski, T., Waltman, P., Zhu, J., Foss, R., Frentzen, B., Friedman, W., McTiernan, R., Yachnis, A., Hayes, D. N., Perou, C. M., Zheng, S., Vegesna, R., Mao, Y., Akbani, R., Aldape, K., Bogler, O., Fuller, G. N., Liu, W., Liu, Y., Lu, Y., Mills, G., Protopopov, A., Ren, X., Sun, Y., Wu, C.-J., Yung, W. K. A., Zhang, W., Zhang, J., Chen, K., Weinstein, J. N., Chin, L., Verhaak, R. G. W., Noushmehr, H., Weisenberger, D. J., Bootwalla, M. S., Lai, P. H., Triche, T. J., Van Den Berg, D. J., Laird, P. W., Gutmann, D. H., Lehman, N. L., VanMeir, E. G., Brat, D., Olson, J. J., Mastrogianakis, G. M., Devi, N. S., Zhang, Z., Bigner, D., Lipp, E., & McLendon, R.
- Affiliations
- Broad Institute (US)
- University Hospital Heidelberg (DE)
- The University of Texas MD Anderson Cancer Center (US)
- Mayo Clinic (US)
- Memorial Sloan Kettering Cancer Center (US)
- Cedars-Sinai Medical Center (US)
- St. Joseph's Hospital and Medical Center (US)
- University of California, San Francisco (US)
- Brigham and Women's Hospital (US)
- Institute for Systems Biology (US)
- Howard Hughes Medical Institute (US)
- Fondazione IRCCS Istituto Neurologico Carlo Besta (IT)
- BC Cancer Agency (CA)
- University of Florida Health (US)
- Penrose-St. Francis Health Services (US)
- University of California, Santa Cruz (US)
- Swedish Medical Center (US)
- Thomas Jefferson University (US)
- University of Southern California (US)
- Washington University in St. Louis (US)
- University Hospitals Cleveland Medical Center (US)
- University of North Carolina at Chapel Hill (US)
- Emory University (US)
- Duke Medical Center (US)
- ORCID
- McKenna, Aaron
- Campos, Benito
- Genovese, Giannicola
- Shukla, Sachet A.
- Guha, Abhijit
- Gibbs, Richard
- Marra, Marco
- Spellman, Paul
- Benz, Christopher
- Ostrom, Quinn
- Xiao, Yonghong
- Auman, J.Todd
- Chen, Peng-Chieh
- Hadjipanayis, Angela
- Lee, Eunjung
- Lee, Semin
- Park, Peter J.
- Seidman, Jonathan
- Yang, Lixing
- Kalkanis, Steven
- Poisson, Laila M.
- Raghunathan, Aditya
- Scarpace, Lisa
- Annala, Matti J.
- Sherman, Mark
- DiMeco, Francesco
- Eoli, Marica
- Maderna, Emanuela
- Pollo, Bianca
- Hoadley, Katherine A.
- Miller, C. Ryan
- Shi, Yan
- Dunn, Gavin
- Giannini, Caterina
- Aksoy, B. Arman
- Borsu, Laetitia
- Cerami, Ethan
- Gao, Jianjiong
- Gross, Benjamin
- Ladanyi, Marc
- Lash, Alex
- Liang, Yupu
- Reva, Boris
- Schultz, Nikolaus
- Shen, Ronglai
- Socci, Nicholas D.
- Viale, Agnes
- Ferguson, Martin L.
- Shaw, Kenna R. Mills
- Sheth, Margi
- Tarnuzzer, Roy
- Yang, Liming
- Davidsen, Tanja
- Ozenberger, Bradley A.
- Sofia, Heidi J.
- Ljubimova, Julia Y.
- Jensen, Mark A.
- Pihl, Todd D.
- Pot, David A.
- Hansen, Nathan
- Lin, Biaoyang
- Shah, Nameeta
- Yoon, Jae-geun
- Lau, Ching
- Berens, Michael
- Ardlie, Kristin
- Carter, Scott L.
- Cherniack, Andrew D.
- Cibulskis, Kristian
- Gehlenborg, Nils
- Heiman, David
- Kim, Jaegil
- Lawrence, Michael
- Lin, Pei
- Saksena, Gordon
- Zhang, Hailei
- Fulton, Lucinda L.
- Fulton, Robert S.
- Mardis, Elaine R.
- Baylin, Stephen B.
- Harshyne, Larry
- Cohen, Mark L.
- VandenBerg, Scott R.
- Berger, Mitchel S.
- Craft, Brian
- Ellrott, Kyle
- Goldman, Mary
- Goldstein, Theodore
- Stuart, Joshua
- Waltman, Peter
- Zhu, Jing
- Yachnis, Anthony
- Mao, Yong
- Akbani, Rehan
- Fuller, Gregory N.
- Liu, Wenbin
- Liu, Yuexin
- Lu, Yiling
- Protopopov, Alexei
- Zhang, Jianhua
- Chen, Ken
- Gutmann, David H.
- Lehman, Norman L.
- Brat, Daniel
- Olson, Jeffrey J.
- Zhang, Zhaobin
- Lipp, Eric
- McLendon, Roger
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2013-10
- Volume
- 155
- Issue
- 2
- Pages
- 462-477
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3910500
- OpenAlex
- W2109816625
- Cited by
- 5,016
- References
- 79
- Citations by year
- 2026: 279 · 2025: 354 · 2024: 397 · 2023: 431 · 2022: 500 · 2021: 520 · 2020: 455 · 2019: 451 · 2018: 373 · 2017: 390 · 2016: 375 · 2015: 295 · 2014: 184 · 2013: 10
- FWCI
- 141.78
- Type
- journal article
- Language
- en
- Update notices
- erratum (2014-04-24)
- Open access
- bronze
- dx.doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- Scholarworks@UNIST (Ulsan National Institute of Science and Technology) (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health (7k08ns045077-06)
- National Human Genome Research Institute (U54HG003067, U54HG003079, U54HG003273)
- National Cancer Institute (P50CA098258, U24CA126554, U24CA143882, U24CA143843, U24CA143840, U24CA126546, U24CA143858, U24CA126543, U24CA144025, U24CA126563, U24CA143866, U24CA143883, U24CA143845, U24CA126544, R01CA163722, U24CA143867, U24CA143848, U24CA143799, P50CA108961, U24CA126551, U24CA143835, U24CA126561, P30CA008748, P30CA015083, P30CA016672, U24CA143731)
- National Institute of Neurological Disorders and Stroke (K08-NS045077)
- 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, somatic alterations, complex chromosomal rearrangements, EGFR, PDGFRA, TERT promoter mutation, telomerase reactivation, proneural subtype, predictive biomarkers, classical subtype, tumor subtypes, proteomic profiling, diagnostic targets
- MeSH terms
- Brain Neoplasms, Female, Glioblastoma, Humans, Male, Mutation, Signal Transduction, Proteome, Gene Expression Profiling, Gene Regulatory Networks
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.
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