ReviewStem cell reviews2008
Glioma formation, cancer stem cells, and akt signaling.
Review in Stem cell reviews, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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
60 citing papers in PubMed.
- H2AX phosphorylation driven by the SET-PP2A axis maintains glioma stem cell properties.Genes & diseases · 2026Article
- Metabolic dependencies and neural progenitor dysregulation: driving forces in paediatric high-grade glioma development.Cancer metastasis reviews · 2026Review
- Preclinical approach of two novel tetrahydroquinoline derivatives targeting GPER and Bcl-2 for anti-glioblastoma therapy.Scientific reports · 2025Article
- Identification of PDLIM1 as a glioblastoma stem cell marker driving tumorigenesis and chemoresistance.Cell death discovery · 2024Article
- Emerging roles of prominin-1 (CD133) in the dynamics of plasma membrane architecture and cell signaling pathways in health and disease.Cellular & molecular biology letters · 2024Review
- A Sequential Targeting Strategy Interrupts AKT-Driven Subclone-Mediated Progression in Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Necrotic reshaping of the glioma microenvironment drives disease progression.Acta neuropathologica · 2022Review
- Knockdown of ETV4 promotes autophagy-dependent apoptosis in GBM cells by reducing the transcriptional activation of EMP1.Oncology letters · 2022Article
- In Silico Analysis of the Correlation of KIF2C with Prognosis and Immune Infiltration in Glioma.Computational and mathematical methods in medicine · 2022Article
- Combined PI3Kα-mTOR Targeting of Glioma Stem Cells.Scientific reports · 2020Article
- Implication of Lactucopicrin in Autophagy, Cell Cycle Arrest and Oxidative Stress to Inhibit U87Mg Glioblastoma Cell Growth.Molecules (Basel, Switzerland) · 2020Article
- Article
- Pharmacological mTOR targeting enhances the antineoplastic effects of selective PI3Kα inhibition in medulloblastoma.Scientific reports · 2019Article
- Endothelial cells promote 3D invasion of GBM by IL-8-dependent induction of cancer stem cell properties.Scientific reports · 2019Article
- Potent Antineoplastic Effects of Combined PI3Kα-MNK Inhibition in Medulloblastoma.Molecular cancer research : MCR · 2019Article
- Potential Strategies Overcoming the Temozolomide Resistance for Glioblastoma.Neurologia medico-chirurgica · 2018Review
- Exploration of Involved Key Genes and Signaling Diversity in Brain Tumors.Cellular and molecular neurobiology · 2018Review
- SC79 protects dopaminergic neurons from oxidative stress.Oncotarget · 2018Article
- Plasticity in Glioma Stem Cell Phenotype and Its Therapeutic Implication.Neurologia medico-chirurgica · 2018Review
- 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
4 authors.
Funding
Abstract
Several recent reports have provided evidence that cancer is initiated by a rare fraction of cells called "cancer stem cells" which are multipotent, self-renewing subset of the tumor. However, several issues regarding the biology and techniques of isolating these cells from solid tumors remain to be clarified. In addition, experimental data supports two possibilities for glioma cell of origin. First, that stem cells or early progenitors are transformed and show variable differentiation of their progeny during tumor development. Second, that more differentiated glia are transformed by genetic events that lead to a loss of differentiation maintenance. In human gliomas, these two theories are not mutually exclusive. In this review we will summarize both theories, and highlight outstanding issues that remain to be resolved.
Indexed as
Identifiers
18595010What 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.