ArticleCell death & disease2020
Identification of a transient state during the acquisition of temozolomide resistance in glioblastoma.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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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.
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Who cites it
48 citing papers in PubMed, 86 citations in OpenAlex.
- Construction of a prognostic model using lactylation-related genes for predicting the prognosis of glioma patients.Medicine · 2026Article
- Construction Strategies, Microenvironmental Modelling and Precision-Therapy Applications of Glioma Organoid Models.Cancers · 2026Review
- Stem-like characteristics across sequentially temozolomide-adapted glioblastoma cell populations with increasing levels of acquired resistance.Molecular biology reports · 2026Article
- MAGMAS Inhibition Enhances Temozolomide Efficacy in Chemotherapy-Resistant Glioblastoma Models.Cancer research communications · 2026Article
- Reprogramming temozolomide response in glioblastoma through regulated and immunogenic cell death modalities.Cell death discovery · 2026Review
- Article
- Single-cell ATAC-seq analysis of human embryoid bodies reveals crucial transcription factor networks involved in early germ layer specification.Cell & bioscience · 2026Article
- Adult spinal cord diffuse midline gliomas with piloid features have a better prognosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- MIRA-1, a p53Molecular biomedicine · 2025Article
- Review
- IDENTIFICATION OF DISEASE-SPECIFIC VULNERABILITY STATES AT THE SINGLE-CELL LEVEL.bioRxiv : the preprint server for biology · 2025Article
- A cell state-specific metabolic vulnerability to GPX4-dependent ferroptosis in glioblastoma.The EMBO journal · 2024Article
- Boric acid Increases Susceptibility to Chemotherapy by Targeting the Ferritinophagy Signaling Pathway in TMZ Resistant Glioblastoma Cells.Biological trace element research · 2024Article
- Glioblastoma Standard of Care: Effects on Tumor Evolution and Reverse Translation in Preclinical Models.Cancers · 2024Review
- VC-resist glioblastoma cell state: vessel co-option as a key driver of chemoradiation resistance.Nature communications · 2024Article
- Modeling stress-induced responses: plasticity in continuous state space and gradual clonal evolution.Theory in biosciences = Theorie in den Biowissenschaften · 2024Article
- Bivalent activity of super-enhancer RNA LINC02454 controls 3D chromatin structure and regulates glioma sensitivity to temozolomide.Cell death & disease · 2024Article
- Overcoming chemotherapy resistance in low-grade gliomas: A computational approach.PLoS computational biology · 2023Article
- Celecoxib Suppresses NF-κB p65 (RelA) and TNFα Expression Signaling in Glioblastoma.Journal of clinical medicine · 2023Article
- MGMT methylation pattern of long-term and short-term survivors of glioblastoma reveals CpGs of the enhancer region to be of high prognostic value.Acta neuropathologica communications · 2023Article
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance limits the therapeutic efficacy in cancers and leads to tumor recurrence through ill-defined mechanisms. Glioblastoma (GBM) are the deadliest brain tumors in adults. GBM, at diagnosis or after treatment, are resistant to temozolomide (TMZ), the standard chemotherapy. To better understand the acquisition of this resistance, we performed a longitudinal study, using a combination of mathematical models, RNA sequencing, single cell analyses, functional and drug assays in a human glioma cell line (U251). After an initial response characterized by cell death induction, cells entered a transient state defined by slow growth, a distinct morphology and a shift of metabolism. Specific genes expression associated to this population revealed chromatin remodeling. Indeed, the histone deacetylase inhibitor trichostatin (TSA), specifically eliminated this population and thus prevented the appearance of fast growing TMZ-resistant cells. In conclusion, we have identified in glioblastoma a population with tolerant-like features, which could constitute a therapeutic target.
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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.