ArticleNeuro-oncology2017
Comprehensive molecular characterization of multifocal glioblastoma proves its monoclonal origin and reveals novel insights into clonal evolution and heterogeneity of glioblastomas.
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 69 papers.
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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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Who cites it
69 citing papers in PubMed, 110 citations in OpenAlex.
- Synchronous Multicentric WHO grade 3 Oligodendroglioma and WHO grade 3 Astrocytoma : A Case Report and Literature Review.Journal of Korean Neurosurgical Society · 2026Article
- Dual TERT promoter mutations in glioblastoma, IDH-wildtype: a case report with preclinical investigations.Brain tumor pathology · 2026Article
- Regrowth Patterns in Glioblastoma-Survival and Predictors.Cancer medicine · 2026Article
- Role of Bevacizumab in Multiple Glioblastomas: A Retrospective Single-Center Analysis.Neurosciences (Riyadh, Saudi Arabia) · 2026Article
- A Case of Multicentric Isocitrate Dehydrogenase-Wildtype Glioblastoma With Divergent Clonal Evolution.Cureus · 2025Article
- Multiomic profiling of glioblastoma metabolic lesions reveals complex intratumoral genomic evolution and dipeptidase-1-driven vascular proliferation.Neuro-oncology · 2025Article
- Chromoanagenesis in Osteosarcoma.Biomolecules · 2025Review
- Discontiguous recurrences of IDH-wildtype glioblastoma share a common origin with the initial tumor and are frequently hypermutated.Acta neuropathologica communications · 2025Article
- Different risk factors for multiple and unifocal gliomas: a comparative study of radiological, pathological and clinical characteristics.Frontiers in oncology · 2025Article
- Efficacy and safety of simultaneous integrated boost intensity-modulated radiotherapy combined with temozolomide for the postoperative chemotherapy treatment of multifocal high-grade glioma.Frontiers in oncology · 2025Article
- Multimodal treatment of glioblastoma with multiple lesions - a multi-center retrospective analysis.Journal of neuro-oncology · 2024Article
- Chromatin Licensing and DNA Replication Factor 1 (CDT1) Is a Potential Prognostic Biomarker Involved in the Malignant Biological Behavior of Glioma.ACS pharmacology & translational science · 2024Article
- Multiple Glioblastomas Ablation by Laser Interstitial Thermal Therapy (LITT): A Rare Case.Cureus · 2024Article
- Sequential Inhibition of PARP and BET as a Rational Therapeutic Strategy for Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Patterns of care and survival in patients with multifocal glioblastoma: A Danish cohort study.Neuro-oncology practice · 2024Article
- Glioma Stem Cells-Features for New Therapy Design.Cancers · 2024Review
- Integrated molecular and multiparametric MRI mapping of high-grade glioma identifies regional biologic signatures.Nature communications · 2023Article
- Glioblastoma heterogeneity at single cell resolution.Oncogene · 2023Review
- Article
- From Theory to Practice: Implementing the WHO 2021 Classification of Adult Diffuse Gliomas in Neuropathology Diagnosis.Brain sciences · 2023Review
9 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The evolution of primary glioblastoma (GBM) is poorly understood. Multifocal GBM (ie, multiple synchronous lesions in one patient) could elucidate GBM development. Methods: We present the first comprehensive study of 12 GBM foci from 6 patients using array-CGH, spectral karyotyping, gene expression arrays, and next-generation sequencing. Results: Multifocal GBMs genetically resemble primary GBMs. Comparing foci from the same patient proved their monoclonal origin. All tumors harbored alterations in the 3 GBM core pathways: RTK/PI3K, p53, and RB regulatory pathways with aberrations of EGFR and CDKN2A/B in all (100%) patients. This unexpected high frequency reflects a distinct genetic signature of multifocal GBMs and might account for their highly malignant and invasive phenotype. Surprisingly, the types of mutations in these genes/pathways were different in tumor foci from the same patients. For example, we found distinct mutations/aberrations in PTEN, TP53, EGFR, and CDKN2A/B, which therefore must have occurred independently and late during tumor development. We also identified chromothripsis as a late event and in tumors with wild-type TP53. Only 2 events were found to be early in all patients: single copy loss of PTEN and TERT promoter point mutations. Conclusions: Multifocal GBMs develop through parallel genetic evolution. The high frequency of alterations in 3 main pathways suggests that these are essential steps in GBM evolution; however, their late occurrence indicates that they are not founder events but rather subclonal drivers. This might account for the marked genetic heterogeneity seen in primary GBM and therefore has important implications for GBM therapy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.