ReviewCell death & disease2016
Glioblastoma, hypoxia and autophagy: a survival-prone 'ménage-à-trois'.
Review in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 1 of them a synthesis that pooled it.
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
101 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.
- Glioblastoma multiforme (GBM): An overview of current therapies and mechanisms of resistance.Pharmacological research · 2021Pooled it
- Mimicking tumor hypoxia in a glioblastoma-on-a-chip.Materials today. Bio · 2026Article
- A stress-adaptive lipid kinase axis defines metabolic vulnerabilities in neuroendocrine prostate cancer.Cancer cell · 2026Article
- Isoliquiritin alleviates sepsis-induced intestinal barrier dysfunction in mice potentially by promoting autophagy.In vitro cellular & developmental biology. Animal · 2026Article
- Prodigiosin Enhanced TMZ Chemosensitivity by Suppressing Focal Adhesion and Inhibiting Autophagy in Glioblastoma Cells.Biomolecules · 2026Article
- Review
- A Stress-Adaptive Lipid Kinase Axis Defines Metabolic Vulnerabilities in Neuroendocrine Prostate Cancer.bioRxiv : the preprint server for biology · 2026Article
- Postoperative ischemia and neurological deficits after glioma resection: A systematic review and meta-analysis.Neuro-oncology practice · 2026Review
- Time-Dependent Effects of Cisplatin on Autophagy Gene Expression in Bladder Cancer Cells.Biomedicines · 2026Article
- Association of Autophagy-Related Gene Expression Profiles with Survival in Diffuse Astrocytic Tumors.Cancers · 2026Article
- Mitochondrial dynamics and cancer: mechanisms and targeted therapy.Cell biology and toxicology · 2026Review
- Biomarkers for predicting immunotherapy response and resistance in glioblastoma.Frontiers in immunology · 2026Review
- Hypoxia response in glioblastoma cells: effect of trehalose on macropinocytosis, autophagy and cell survival.Biochemistry and biophysics reports · 2025Article
- Mitochondrial connexin 43 modulates metabolic stress adaptation in glioma cell lines.Cell communication and signaling : CCS · 2025Article
- Atypical cadherin FAT1 promotes tumorigenesis by suppressing autophagic cell death in glioblastoma under hypoxia or nutrient stress.Cellular & molecular biology letters · 2025Article
- Multi-omics analysis identifies novels genes involved in glioma prognosis.Scientific reports · 2025Article
- Targeting the Interplay Between Autophagy and the Nrf2 Pathway in Parkinson's Disease with Potential Therapeutic Implications.Biomolecules · 2025Review
- Autophagy in brain tumors: molecular mechanisms, challenges, and therapeutic opportunities.Journal of translational medicine · 2025Review
- The neglected burden of chronic hypoxia on the resistance of glioblastoma multiforme to first-line therapies.BMC biology · 2024Review
- Hypoxia-Responsive Prodrug of ATR Inhibitor, AZD6738, Selectively Eradicates Treatment-Resistant Cancer Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
41 more citing papers are in PubMed but not listed here.
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
Glioblastoma multiforme is the most common and the most aggressive primary brain tumor. It is characterized by a high degree of hypoxia and also by a remarkable resistance to therapy because of its adaptation capabilities that include autophagy. This degradation process allows the recycling of cellular components, leading to the formation of metabolic precursors and production of adenosine triphosphate. Hypoxia can induce autophagy through the activation of several autophagy-related proteins such as BNIP3, AMPK, REDD1, PML, and the unfolded protein response-related transcription factors ATF4 and CHOP. This review summarizes the most recent data about induction of autophagy under hypoxic condition and the role of autophagy in glioblastoma.
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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.