ReviewFrontiers in oncology2020
Genetic Architectures and Cell-of-Origin in Glioblastoma.
Review in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 61 citations in OpenAlex.
- EGFRvIII Reduces Neural Stem/Progenitor Marker Expression in GFAP-Negative iNSCs: Evidence for a Context-Dependent Cellular Response.International journal of molecular sciences · 2026Article
- Putative glioblastoma origin-like cells in the subventricular zone: isolation and characterization.Experimental & molecular medicine · 2026Article
- Overcoming Chemoresistance in Glioblastoma: Mechanisms, Therapeutic Strategies, and Functional Precision Medicine.International journal of molecular sciences · 2026Review
- Genetic landscape of cancer: mechanisms, key genes, and therapeutic implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Connexin-Pannexin duality in glioblastoma.Cell and tissue research · 2026Review
- Bridging MBD3 functions in developmental biology and glioma heterogeneity to immune remodeling with future perspectives.Frontiers in immunology · 2026Review
- FOLR1 Regulates the Malignant Progression of Glioblastoma through the SRC/ERK1/2 Axis.Combinatorial chemistry & high throughput screening · 2026Article
- Bioengineering Stem Cell-Derived Glioblastoma Organoids: A Comprehensive Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Glioblastoma: From Pathophysiology to Novel Therapeutic Approaches.Biomedicines · 2025Review
- Integrating Radiogenomics and Machine Learning in Musculoskeletal Oncology Care.Diagnostics (Basel, Switzerland) · 2025Review
- scMalignantFinder distinguishes malignant cells in single-cell and spatial transcriptomics by leveraging cancer signatures.Communications biology · 2025Article
- Radiogenomics and machine learning predict oncogenic signaling pathways in glioblastoma.Journal of translational medicine · 2025Article
- CAR-T cell therapy in brain malignancies: obstacles in the face of cellular trafficking and persistence.Frontiers in immunology · 2025Review
- Integrating molecular profiling into glioma diagnosis: implications of the WHO-CNS5-2021 classification of adult-type diffuse gliomas in Colombian patients.Frontiers in neurology · 2025Article
- Article
- A triple hormone receptor ER, AR, and VDR signature is a robust prognosis predictor in breast cancer.Breast cancer research : BCR · 2024Article
- Circulating Liquid Biopsy Biomarkers in Glioblastoma: Advances and Challenges.International journal of molecular sciences · 2024Review
- Sphingolipid Signaling and Complement Activation in Glioblastoma: A Promising Avenue for Therapeutic Intervention.BioChem · 2024Article
- MiR-128-3p - a gray eminence of the human central nervous system.Molecular therapy. Nucleic acids · 2024Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An aggressive primary brain cancer, glioblastoma (GBM) is the most common cancer of the central nervous system in adults. However, an inability to identify its cell-of-origin has been a fundamental issue hindering further understanding of the nature and pathogenesis of GBM, as well as the development of novel therapeutic targets. Researchers have hypothesized that GBM arises from an accumulation of somatic mutations in neural stem cells (NSCs) and glial precursor cells that confer selective growth advantages, resulting in uncontrolled proliferation. In this review, we outline genomic perspectives on IDH-wildtype and IDH-mutant GBMs pathogenesis and the cell-of-origin harboring GBM driver mutations proposed by various GBM animal models. Additionally, we discuss the distinct neurodevelopmental programs observed in either IDH-wildtype or IDH-mutant GBMs. Further research into the cellular origin and lineage hierarchy of GBM will help with understanding the evolution of GBMs and with developing effective targets for treating GBM cancer cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.