SynthesisActa neuropathologica2018
Reconstructing the molecular life history of gliomas.
Synthesis in Acta neuropathologica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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.
The trial behind it
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
58 citing papers in PubMed.
- Exploring the landscape of targetable alterations in patients with glioblastoma.Nature reviews. Clinical oncology · 2026Review
- Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Dual TERT promoter mutations in glioblastoma, IDH-wildtype: a case report with preclinical investigations.Brain tumor pathology · 2026Article
- Telomere Dysfunction in Human Astrocytes Drives Acrocentric Chromosome Instability and Nucleolar Reorganization.bioRxiv : the preprint server for biology · 2026Article
- Chromosome-arm-specific telomere length governs dual modes of structural genome evolution in IDH-mutant astrocytoma.bioRxiv : the preprint server for biology · 2026Article
- Unraveling the role of specificity protein 1 in gliomas: pathophysiology and clinical implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Multiomic profiling of glioblastoma metabolic lesions reveals complex intratumoral genomic evolution and dipeptidase-1-driven vascular proliferation.Neuro-oncology · 2025Article
- Evolutionary trajectories of IDH-mutant astrocytoma identify molecular grading markers related to cell cycling.Nature cancer · 2025Article
- Cell sorting based on single nucleotide variation enables characterization of mutation-dependent transcriptome and chromatin states.Nucleic acids research · 2025Article
- Management and survival trends for diffuse gliomas diagnosed at a single neurooncology center in China during 2000 to 2020.Scientific reports · 2025Article
- Actionable alterations in glioblastoma: Insights from the implementation of genomic profiling as the standard of care from 2016 to 2023.Neuro-oncology practice · 2025Article
- Longitudinal multimodal profiling of IDH-wildtype glioblastoma reveals the molecular evolution and cellular phenotypes underlying prognostically different treatment responses.Neuro-oncology · 2025Article
- Bioinformatic and clinical experimental assay uncovers resistance and susceptibility mechanisms of human glioblastomas to temozolomide and identifies new combined and individual survival biomarkers outperformingTherapeutic advances in medical oncology · 2024Article
- Article
- Integrated molecular and multiparametric MRI mapping of high-grade glioma identifies regional biologic signatures.Nature communications · 2023Article
- Distinct aneuploid evolution of astrocytoma and glioblastoma during recurrence.NPJ precision oncology · 2023Article
- Genomic profiles of IDH-mutant gliomas: MYCN-amplified IDH-mutant astrocytoma had the worst prognosis.Scientific reports · 2023Article
- Rewired mNature communications · 2023Article
- Molecular landscape of IDH-wild type, pTERT-wild type adult glioblastomas.Brain pathology (Zurich, Switzerland) · 2022Article
- EID3 Promotes Glioma Cell Proliferation and Survival by Inactivating AMPKα1.Journal of Korean Neurosurgical Society · 2022Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
At the time of their clinical manifestation, the heterogeneous group of adult and pediatric gliomas carries a wide range of diverse somatic genomic alterations, ranging from somatic single-nucleotide variants to structural chromosomal rearrangements. Somatic abnormalities may have functional consequences, such as a decrease, increase or change in mRNA transcripts, and cells pay a penalty for maintaining them. These abnormalities, therefore, must provide cells with a competitive advantage to become engrained into the glioma genome. Here, we propose a model of gliomagenesis consisting of the following five consecutive phases that glioma cells have traversed prior to clinical manifestation: (I) initial growth; (II) oncogene-induced senescence; (III) stressed growth; (IV) replicative senescence/crisis; (V) immortal growth. We have integrated the findings from a large number of studies in biology and (neuro)oncology and relate somatic alterations and other results discussed in these papers to each of these five phases. Understanding the story that each glioma tells at presentation may ultimately facilitate the design of novel, more effective therapeutic approaches.
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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.