ArticleNeuro-oncology2016
Comparative genomic and genetic analysis of glioblastoma-derived brain tumor-initiating cells and their parent tumors.
Article in Neuro-oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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
29 citing papers in PubMed.
- Multi-sampling allows intra-tumoral heterogeneity querying and vulnerability profiling in glioblastoma.Neuro-oncology · 2026Article
- A novel disulfide death-related genes prognostic signature identifies the role of IPO4 in glioma progression.Cancer cell international · 2024Article
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- Establishment and Comprehensive Molecular Characterization of an Immortalized Glioblastoma Cell Line from a Brazilian Patient.International journal of molecular sciences · 2023Article
- Ex vivo drug sensitivity screening predicts response to temozolomide in glioblastoma patients and identifies candidate biomarkers.British journal of cancer · 2023Article
- Oncolytic herpes simplex viruses for the treatment of glioma and targeting glioblastoma stem-like cells.Frontiers in cellular and infection microbiology · 2023Review
- Preservation of the Hypoxic Transcriptome in Glioblastoma Patient-Derived Cell Lines Maintained at Lowered Oxygen Tension.Cancers · 2022Article
- Glioblastoma, from disease understanding towards optimal cell-based in vitro models.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- CD95 gene deletion may reduce clonogenic growth and invasiveness of human glioblastoma cells in a CD95 ligand-independent manner.Cell death discovery · 2022Article
- Anti-glioblastoma effects of phenolic variants of benzoylphenoxyacetamide (BPA) with high potential for blood brain barrier penetration.Scientific reports · 2022Article
- Article
- Tumor-targeting cell-penetrating peptide, p28, for glioblastoma imaging and therapy.Frontiers in oncology · 2022Article
- A Novel Defined Endoplasmic Reticulum Stress-Related lncRNA Signature for Prognosis Prediction and Immune Therapy in Glioma.Frontiers in oncology · 2022Article
- Tumor heterogeneity assessed by sequencing and fluorescence in situ hybridization (FISH) data.Bioinformatics (Oxford, England) · 2021Article
- Article
- Glioma-derived IL-33 orchestrates an inflammatory brain tumor microenvironment that accelerates glioma progression.Nature communications · 2020Article
- In silico identification of the prognostic biomarkers and therapeutic targets associated with cancer stem cell characteristics of glioma.Bioscience reports · 2020Article
- Tumor Copy Number Deconvolution Integrating Bulk and Single-Cell Sequencing Data.Journal of computational biology : a journal of computational molecular cell biology · 2020Article
- Genomic and Phenotypic Characterization of a Broad Panel of Patient-Derived Xenografts Reflects the Diversity of Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastoma (GBM) is a fatal cancer that has eluded major therapeutic advances. Failure to make progress may reflect the absence of a human GBM model that could be used to test compounds for anti-GBM activity. In this respect, the development of brain tumor-initiating cell (BTIC) cultures is a step forward because BTICs appear to capture the molecular diversity of GBM better than traditional glioma cell lines. Here, we perform a comparative genomic and genetic analysis of BTICs and their parent tumors as preliminary evaluation of the BTIC model.
methodsWe assessed single nucleotide polymorphisms (SNPs), genome-wide copy number variations (CNVs), gene expression patterns, and molecular subtypes of 11 established BTIC lines and matched parent tumors.
resultsAlthough CNV differences were noted, BTICs retained the major genomic alterations characteristic of GBM. SNP patterns were similar between BTICs and tumors. Importantly, recurring SNP or CNV alterations specific to BTICs were not seen. Comparative gene expression analysis and molecular subtyping revealed differences between BTICs and GBMs. These differences formed the basis of a 63-gene expression signature that distinguished cells from tumors; differentially expressed genes primarily involved metabolic processes. We also derived a set of 73 similarly expressed genes; these genes were not associated with specific biological functions.
conclusionsAlthough not identical, established BTIC lines preserve the core molecular alterations seen in their parent tumors, as well as the genomic hallmarks of GBM, without acquiring recurring BTIC-specific changes.
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