{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wang LB"],"funding":["U.S. Department of Energy","NIEHS NIH HHS","NHGRI NIH HHS","National Cancer Institute","NCI NIH HHS","NINDS NIH HHS","National Institutes of Health","National Human Genome Research Institute"],"pagination":["509-528.e20"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8044053"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["39(4)"],"pubmed_abstract":["Glioblastoma (GBM) is the most aggressive nervous system cancer. Understanding its molecular pathogenesis is crucial to improving diagnosis and treatment. Integrated analysis of genomic, proteomic, post-translational modification and metabolomic data on 99 treatment-naive GBMs provides insights to GBM biology. We identify key phosphorylation events (e.g., phosphorylated PTPN11 and PLCG1) as potential switches mediating oncogenic pathway activation, as well as potential targets for EGFR-, TP53-, and RB1-altered tumors. Immune subtypes with distinct immune cell types are discovered using bulk omics methodologies, validated by snRNA-seq, and correlated with specific expression and histone acetylation patterns. Histone H2B acetylation in classical-like and immune-low GBM is driven largely by B"],"journal":["Cancer cell"],"pubmed_title":["Proteogenomic and metabolomic characterization of human glioblastoma."],"pmcid":["PMC8044053"],"funding_grant_id":["U24 CA160019","P30 ES010126","U24 CA210967","U24 CA210979","U24 CA210954","U24 CA210955","R01 HG009711","U24 CA210985","U24 CA210986","R01 NS107833","U24 CA210972","K08 NS102474","U24 CA210993","U01 CA214125","T32 HG000045"],"pubmed_authors":["Sieh W","Jewell SD","Pruetz B","Traer E","Calinawan AP","Moore RJ","Kinsinger CR","Hanhan Z","Suh J","Gabrovski N","Newton CJ","Monroe ME","Maunganidze N","Paulovich AG","Rodland KD","McDermott JE","Wilson GD","Carr SA","Borate U","Kawaler E","Modugno F","D'Angelo F","Madan R","Krug K","Fenyo D","Qi L","Lei J","Smith RD","Vatanian N","Dhir R","Valley DR","Hannick LI","Bramer LM","Hiltke T","Zhao R","Zhao G","Schurer S","Roche N","Ruggles KV","Marrero-Oliveras A","Mareedu S","Zhu H","Gritsenko MA","Chinnaiyan AM","Zhu J","Hindenach B","Cao S","Kyle JE","Henderson BL","Hong R","Bocik WE","Stratton KG","Ceccarelli M","Pugliese P","Colaprico A","Couvillion SP","Wang LB","Cottingham SL","Agarwal A","Tabor D","Skelly T","Chesla D","Omenn GS","Wiznerowicz M","Mieczkowski P","Bloodsworth KJ","Francis A","Chen F","Li K","Golbin D","Thangudu RR","Ketchum KA","Cerda S","Li Y","Birger C","Kaspera W","Martinez N","Birrer MJ","Dhanasekaran SM","Kumar-Sinha C","Moon J","Liu H","Cai S","Liu T","Migliozzi S","Kim AH","Lilly J","Liu W","Ma W","Gillette MA","Zelt R","Petralia F","Kothadia RB","Clark DJ","Polonskaya L","Riggins G","Thiagarajan M","Paklina OV","Mani DR","Godwin AK","Vasaikar S","Maggio W","Savage SR","Domagalski MJ","Blumenberg L","Rothstein JH","Zhang Z","Yoo S","Weitz KK","Mesri M","Burke MC","Culpepper H","Stein SE","Wyczalkowski MA","Zhang H","Zhang L","Lubinski J","Shi Z","Wan W","Shi Y","Um KS","Karpova A","Dou Y","Duffy E","Robles AI","Resnick AC","Zakhartsev Y","Chen XS","Bauer T","Montgomery R","Velvulou U","Zhang B","Tsang S","Boekweg H","Li QK","Edwards R","Cui Zhou D","Pico AR","Wendl MC","Boja ES","An E","Dyer M","Potapova O","Eschbacher J","Placantonakis DG","Rykunov D","Satpathy S","Stathias V","Nesvizhskii AI","Krek A","Amin M","Ozbek U","Chan DW","Druker B","Ramkissoon S","Demir E","Kim L","Day J","Rood BR","Vernon M","Reva B","Tsai CF","Karz A","Hariharan P","Baral J","Demopoulos A","Whiteaker JR","Leprevost FD","Borucki M","Edwards NJ","Jones CD","Rohrer DC","Boca SM","De Young S","Schadt EE","Elburn K","Shutack Y","Caravan W","Malc E","Chen LS","Huang C","Richey S","Payne SH","Chu RK","Wang J","Lindgren CM","Jaehnig E","Wang P","Szopa W","Gabriel S","Wen B","Olsen LK","Singh S","Wu Y","Resnick A","Yao L","Garofano L","Liao Y","Stawicki J","Sokoll LJ","Tan D","Cornwell M","Webster A","Barnholtz-Sloan JS","Yang X","Markey SP","Lu S","Charamut A","Clinical Proteomic Tumor Analysis Consortium","Hostetter G","Tognon C","McMichael JF","Tansil D","Tyner J","Perou AM","Rodriguez H","Iavarone A","Getz G","Hoadley KA","Liang WW","Chowdhury S","Andrews DW","McGarvey PB","Rossell L","Ding L","Anderson ML","Piehowski PD","Song X","McGee J","Robinson K","Chheda MG","Ji J","Ji N","Petyuk VA","Malovannaya A","Czernicki T","Ellis MJ","Cieslik MP","Zink E"],"additional_accession":[]},"is_claimable":false,"name":"Proteogenomic and metabolomic characterization of human glioblastoma.","description":"Glioblastoma (GBM) is the most aggressive nervous system cancer. Understanding its molecular pathogenesis is crucial to improving diagnosis and treatment. Integrated analysis of genomic, proteomic, post-translational modification and metabolomic data on 99 treatment-naive GBMs provides insights to GBM biology. We identify key phosphorylation events (e.g., phosphorylated PTPN11 and PLCG1) as potential switches mediating oncogenic pathway activation, as well as potential targets for EGFR-, TP53-, and RB1-altered tumors. Immune subtypes with distinct immune cell types are discovered using bulk omics methodologies, validated by snRNA-seq, and correlated with specific expression and histone acetylation patterns. Histone H2B acetylation in classical-like and immune-low GBM is driven largely by B","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Apr","modification":"2026-05-02T22:46:09.727Z","creation":"2025-04-04T22:13:08.015Z"},"accession":"S-EPMC8044053","cross_references":{"pubmed":["33577785"],"doi":["10.1016/j.ccell.2021.01.006"]}}