ArticleJournal of neuro-oncology2012
Hyperoxia resensitizes chemoresistant human glioblastoma cells to temozolomide.
Article in Journal of neuro-oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 42 citations in OpenAlex.
- Novel desensitization protocol utilizing conventional formulations to mitigate Temozolomide-Related skin hypersensitivity.Cancer chemotherapy and pharmacology · 2025Article
- Key Genes Involved in the Beneficial Mechanism of Hyperbaric Oxygen for Glioblastoma and Predictive Indicators of Hyperbaric Oxygen Prolonging Survival in Glioblastoma Patients.Current medical science · 2024Article
- c-MET and the immunological landscape of cancer: novel therapeutic strategies for enhanced anti-tumor immunity.Frontiers in immunology · 2024Review
- Dodecafluoropentane Emulsion as a Radiosensitizer in Glioblastoma Multiforme.Cancer research communications · 2023Article
- Review
- Prodrugs of a 1-Hydroxy-2-oxopiperidin-3-yl Phosphonate Enolase Inhibitor for the Treatment ofJournal of medicinal chemistry · 2022Article
- Hypoxia-inducible lentiviral gene expression in engineered human macrophages.Journal for immunotherapy of cancer · 2022Article
- Implications of Hyperoxia over the Tumor Microenvironment: An Overview Highlighting the Importance of the Immune System.Cancers · 2022Review
- Exploring Hyperoxia Effects in Cancer-From Perioperative Clinical Data to Potential Molecular Mechanisms.Biomedicines · 2021Review
- Glioblastoma Metabolomics-In Vitro Studies.Metabolites · 2021Review
- Article
- Role of hyperoxic treatment in cancer.Experimental biology and medicine (Maywood, N.J.) · 2020Review
- Role of NKCC1 Activity in Glioma KFrontiers in physiology · 2020Article
- Hyperbaric oxygen increases glioma cell sensitivity to antitumor treatment with a novel isothiourea derivative in vitro.Oncology reports · 2019Article
- Mild thermotherapy and hyperbaric oxygen enhance sensitivity of TMZ/PSi nanoparticles via decreasing the stemness in glioma.Journal of nanobiotechnology · 2019Article
- Hyperbaric oxygen inhibits production of CD3+ T cells in the thymus and facilitates malignant glioma cell growth.The Journal of international medical research · 2018Article
- Overcoming tumor hypoxia as a barrier to radiotherapy, chemotherapy and immunotherapy in cancer treatment.International journal of nanomedicine · 2018Review
- Endoplasmic reticulum chaperone prolyl 4-hydroxylase, beta polypeptide (P4HB) promotes malignant phenotypes in glioma via MAPK signaling.Oncotarget · 2017Article
- Endoplasmic reticulum stress signaling and chemotherapy resistance in solid cancers.Oncogenesis · 2017Review
- HIF1α regulates glioma chemosensitivity through the transformation between differentiation and dedifferentiation in various oxygen levels.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Temozolomide (TMZ) is standard chemotherapy for glioblastoma multiforme (GBM). Intratumoral hypoxia is common in GBM and may be associated with the development of TMZ resistance. Oxygen therapy has previously been reported to potentiate the effect of chemotherapy in cancer. In this study, we investigated whether hyperoxia can enhance the TMZ-induced cytotoxicity of human GBM cells, and whether and how it would resensitize TMZ-resistant GBM cells to TMZ. TMZ-sensitive human GBM cells (D54-S and U87-S) were treated with TMZ to develop isogenic subclones of TMZ-resistant cells (D54-R and U87-R). All cell lines were then exposed to different oxygen levels (1, 21, 40, or 80 %), with or without concomitant TMZ treatment, before assessment of cell cytotoxicity and morphology. Cell death and survival pathways elicited by TMZ and/or hyperoxia were elucidated by western blotting. Our results showed that TMZ sensitivity of both chemo-sensitive and resistant cells was enhanced significantly under hyperoxia. At the cell line-specific optimum oxygen concentration (D54-R, 80 %; U87-R, 40 %), resistant cells had the same response to TMZ as the parent chemosensitive cells under normoxia via the caspase-dependent pathway. Both TMZ and hyperoxia were associated with increased phosphorylation of ERK p44/42 MAPK (Erk1/2), but to a lesser extent in D54-R cells, suggesting that Erk1/2 activity may be involved in regulation of hyperoxia and TMZ-mediated cell death. Overall, hyperoxia enhanced TMZ toxicity in GBM cells by induction of apoptosis, possibly via MAPK-related pathways. Induced hyperoxia is a potentially promising approach for treatment of TMZ-resistant GBM.
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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.