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Publication

An Integrative Model of Cellular States, Plasticity, and Genetics for Glioblastoma.

Cyril Neftel | Julie Laffy | Mariella G Filbin | Toshiro Hara | Marni E Shore | Gilbert J Rahme | Alyssa R Richman | Dana Silverbush | McKenzie L Shaw | Christine M Hebert | John Dewitt | Simon Gritsch | Elizabeth M Perez | L Nicolas Gonzalez Castro | Xiaoyang Lan | Nicholas Druck | Christopher Rodman | Danielle Dionne | Alexander Kaplan | Mia S Bertalan | Julia Small | Kristine Pelton | Sarah Becker | Dennis Bonal | Quang-De Nguyen | Rachel L Servis | Jeremy M Fung | Ravindra Mylvaganam | Lisa Mayr | Johannes Gojo | Christine Haberler | Rene Geyeregger | Thomas Czech | Irene Slavc | Brian V Nahed | William T Curry | Bob S Carter | Hiroaki Wakimoto | Priscilla K Brastianos | Tracy T Batchelor | Anat Stemmer-Rachamimov | Maria Martinez-Lage | Matthew P Frosch | Ivan Stamenkovic | Nicolo Riggi | Esther Rheinbay | Michelle Monje | Orit Rozenblatt-Rosen | Daniel P Cahill | Anoop P Patel | Tony Hunter | Inder M Verma | Keith L Ligon | David N Louis | Aviv Regev | Bradley E Bernstein | Itay Tirosh | Mario L Suvà
Cell | 2019

Diverse genetic, epigenetic, and developmental programs drive glioblastoma, an incurable and poorly understood tumor, but their precise characterization remains challenging. Here, we use an integrative approach spanning single-cell RNA-sequencing of 28 tumors, bulk genetic and expression analysis of 401 specimens from the The Cancer Genome Atlas (TCGA), functional approaches, and single-cell lineage tracing to derive a unified model of cellular states and genetic diversity in glioblastoma. We find that malignant cells in glioblastoma exist in four main cellular states that recapitulate distinct neural cell types, are influenced by the tumor microenvironment, and exhibit plasticity. The relative frequency of cells in each state varies between glioblastoma samples and is influenced by copy number amplifications of the CDK4, EGFR, and PDGFRA loci and by mutations in the NF1 locus, which each favor a defined state. Our work provides a blueprint for glioblastoma, integrating the malignant cell programs, their plasticity, and their modulation by genetic drivers.

Pubmed ID: 31327527

Research resources used in this publication

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Antibodies used in this publication

Associated grants

  • Agency: NCI NIH HHS, United States
    Id: DP1 CA216873
  • Agency: NCI NIH HHS, United States
    Id: U24 CA180922
  • Agency: NCI NIH HHS, United States
    Id: P30 CA014051
  • Agency: NCI NIH HHS, United States
    Id: K12 CA090354
  • Agency: NCI NIH HHS, United States
    Id: R01 CA195613
  • Agency: NCI NIH HHS, United States
    Id: R33 CA202820
  • Agency: NCI NIH HHS, United States
    Id: P30 CA014195
  • Agency: NIGMS NIH HHS, United States
    Id: T32 GM080177
  • Agency: NCRR NIH HHS, United States
    Id: S10 RR023440
  • Agency: NCI NIH HHS, United States
    Id: F32 CA236432
  • Agency: NIH HHS, United States
    Id: S10 OD023689
  • Agency: NCI NIH HHS, United States
    Id: P50 CA165962
  • Agency: Howard Hughes Medical Institute, United States

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