ArticleNeuro-oncology2017
Multi-omics analysis of primary glioblastoma cell lines shows recapitulation of pivotal molecular features of parental tumors.
Article in Neuro-oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 47 citations in OpenAlex.
- Attract to kill: Exploring the potential of motility trapping as a novel treatment strategy for high-grade gliomas.Neuro-oncology · 2026Review
- Modelling brain tumours with organoids: towards precision medicine in neuro-oncology.Nature reviews. Neurology · 2026Review
- Article
- Nicotinamide metabolism reprogramming drives reversible senescence of glioblastoma cells.Cellular and molecular life sciences : CMLS · 2025Article
- Microtubule-associated NAV3 regulates invasive phenotypes in glioblastoma cells.Brain pathology (Zurich, Switzerland) · 2025Article
- Single-cell profiling and zebrafish avatars reveal LGALS1 as immunomodulating target in glioblastoma.EMBO molecular medicine · 2023Article
- Single-cell molecular profiling using ex vivo functional readouts fuels precision oncology in glioblastoma.Cellular and molecular life sciences : CMLS · 2023Article
- Genome-wide profiling of patient-derived glioblastoma stem-like cells reveals recurrent genetic and transcriptomic signatures associated with brain tumors.Journal of neuro-oncology · 2023Article
- Oncolytic herpes simplex viruses for the treatment of glioma and targeting glioblastoma stem-like cells.Frontiers in cellular and infection microbiology · 2023Review
- Lipidomics combined with transcriptomic and mass spectrometry imaging analysis of the Asiatic toad (Bufo gargarizans) during metamorphosis and bufadienolide accumulation.Chinese medicine · 2022Article
- Glioblastoma cell motility depends on enhanced oxidative stress coupled with mobilization of a sulfurtransferase.Cell death & disease · 2022Article
- PTEN inhibits AMPK to control collective migration.Nature communications · 2022Article
- Functional Precision Oncology: The Next Frontier to Improve Glioblastoma Outcome?International journal of molecular sciences · 2022Review
- Targeting Acid Ceramidase Inhibits Glioblastoma Cell Migration through Decreased AKT Signaling.Cells · 2022Article
- Article
- PAK3 is a key signature gene of the glioma proneural subtype and affects its proliferation, differentiation and growth.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Heterogeneity of Response to Iron-Based Metallodrugs in Glioblastoma Is Associated with Differences in Chemical Structures and Driven by FAS Expression Dynamics and Transcriptomic Subtypes.International journal of molecular sciences · 2021Article
- Transcriptional CDK inhibitors, CYC065 and THZ1 promote Bim-dependent apoptosis in primary and recurrent GBM through cell cycle arrest and Mcl-1 downregulation.Cell death & disease · 2021Article
- Marizomib sensitizes primary glioma cells to apoptosis induced by a latest-generation TRAIL receptor agonist.Cell death & disease · 2021Article
- A New Era of Neuro-Oncology Research Pioneered by Multi-Omics Analysis and Machine Learning.Biomolecules · 2021Review
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Glioblastoma (GBM) is the deadliest primary brain cancer in adults. Emerging innovative therapies hold promise for personalized cancer treatment. Improving therapeutic options depends on research relying on relevant preclinical models. In this line we have established in the setting of the GlioTex project (GBM and Experimental Therapeutics) a GBM patient-derived cell line (GBM-PDCL) library. A multi-omic approach was used to determine the molecular landscape of PDCL and the extent to which they represent GBM tumors. Methods: Single nucleotide polymorphism array, expression arrays, exome sequencing, and RNA sequencing were used to measure and compare the molecular landscapes of 20 samples representing 10 human GBM tumors and paired GBM-PDCLs. Results: Copy number variations were similar for a median of 85% of the genome and for 59% of the major focal events. Somatic point mutations were similar in a median of 41%. Mutations in GBM driver and "druggable" genes were maintained in 67% of events. Mutations that were not conserved in the PDCL were mainly low allelic fraction and/or non-driver mutations. Based on RNA expression profiling, PDCLs cluster closely to their parental tumor with overexpression of pathways associated with cancer progression in PDCL. Conclusions: Overall, PDCLs recapitulate pivotal molecular alterations of paired-parental tumors supporting their use as a preclinical model of GBM. However, some driver aberrations are lost or gained in the passage from tumor to PDCL. Our results support using PDCL as a relevant preclinical model of GBM. Further investigations of changes between PDCLs and their parental tumor may provide insights into GBM biology.
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