ReviewCancers2023
The Role of Hypoxia and Cancer Stem Cells in Development of Glioblastoma.
Review in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 42 citations in OpenAlex.
- Pathway dysregulation and therapeutic resistance in glioblastoma: molecular mechanisms and emerging therapeutic targets.Future science OA · 2026Review
- Breaking adaptive oncogenic resistance in glioblastoma via targeting the EGFR-STAT3 axis.Medical oncology (Northwood, London, England) · 2026Review
- Review
- Precision Immunotherapeutics for Glioblastoma: Current Approaches and Emerging Strategies in 2026.Cells · 2026Review
- Glioblastoma Stem Cells and Tumour Microenvironment: Interactions Across Hypoxia, Vasculature and Immune Modulation.International journal of molecular sciences · 2026Review
- Review
- Glioblastoma as a neuro-immune network disorder: rethinking the tumor microenvironment, neural circuit integration, and therapeutic resistance.Oncology reviews · 2026Review
- Revealing erythropoietin variant EV-3 as novel driving force and immunotherapeutic target in human glioblastoma.Journal of experimental & clinical cancer research : CR · 2025Article
- Glioblastoma insights: Focus on crosstalk with the suppressive tumor microenvironment and advanced therapeutic strategies.Medicine · 2025Review
- Hypoxia response in glioblastoma cells: effect of trehalose on macropinocytosis, autophagy and cell survival.Biochemistry and biophysics reports · 2025Article
- Selective regulation and cellular metabolism by the lactate transporter MCT4 in GBM.Medical oncology (Northwood, London, England) · 2025Article
- HIF-1α and HIF-2α: synergistic regulation of glioblastoma malignant progression during hypoxia and apparent chemosensitization in response to hyperbaric oxygen.Cancer cell international · 2025Article
- The Complexity of Malignant Glioma Treatment.Cancers · 2025Review
- Exploring miRNA therapies and gut microbiome-enhanced CAR-T cells: advancing frontiers in glioblastoma stem cell targeting.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Hyperbaric oxygen promotes both the proliferation and chemosensitization of glioblastoma cells by inhibiting HIF1α/HIF2α-ABCG2.Frontiers in molecular neuroscience · 2025Article
- Exploring a new direction in targeted cancer therapy through hyperbaric oxygen therapy combined with biomedical engineering techniques.Frontiers in oncology · 2025Review
- Nano-biomaterials in cancer therapy: Advances in targeting and overcoming cancer stem cell resistance.ADMET & DMPK · 2025Review
- Metabolism of glioblastoma: a review of metabolic adaptations and metabolic therapeutic interventions.Frontiers in oncology · 2025Review
- Comprehensive review of drug resistance in mammalian cancer stem cells: implications for cancer therapy.Cancer cell international · 2024Review
- The neglected burden of chronic hypoxia on the resistance of glioblastoma multiforme to first-line therapies.BMC biology · 2024Review
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 at 1 institution in 1 country.
Funding
Abstract
Glioblastoma multiform (GBM) is recognized as the most malignant brain tumor with a high level of hypoxia, containing a small population of glioblastoma stem like cells (GSCs). These GSCs have the capacity of self-renewal, proliferation, invasion and recapitulating the parent tumor, and are major causes of radio-and chemoresistance of GBM. Upregulated expression of hypoxia inducible factors (HIFs) in hypoxia fundamentally contributes to maintenance and progression of GSCs. Therefore, we thoroughly reviewed the currently acknowledged roles of hypoxia-associated GSCs in development of GBM. In detail, we recapitulated general features of GBM, especially GSC-related features, and delineated essential responses resulted from interactions between GSC and hypoxia, including hypoxia-induced signatures, genes and pathways, and hypoxia-regulated metabolic alterations. Five hypothesized GSC niches are discussed and integrated into one comprehensive concept: hypoxic peri-arteriolar niche of GSCs. Autophagy, another protective mechanism against chemotherapy, is also closely related to hypoxia and is a potential therapeutic target for GBM. In addition, potential causes of therapeutic resistance (chemo-, radio-, surgical-, immuno-), and chemotherapeutic agents which can improve the therapeutic effects of chemo-, radio-, or immunotherapy are introduced and discussed. At last, as a potential approach to reverse the hypoxic microenvironment in GBM, hyperbaric oxygen therapy (HBOT) might be an adjuvant therapy to chemo-and radiotherapy after surgery. In conclusion, we focus on demonstrating the important role of hypoxia on development of GBM, especially by affecting the function of GSCs. Important advantages have been made to understand the complicated responses induced by hypoxia in GBM. Further exploration of targeting hypoxia and GSCs can help to develop novel therapeutic strategies to improve the survival of GBM patients.
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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.