ArticleiScience2020
Oncogenic Gain of Function in Glioblastoma Is Linked to Mutant p53 Amyloid Oligomers.
Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Multi-Site Aggregation of p53: Insights from Self- and Co-Aggregation of Multiple Aggregation-Prone Regions.ACS omega · 2026Article
- Reactivation ofInternational journal of molecular sciences · 2026Article
- Cancer-linked aggregation of p53 is driven by sequence-encoded frustration, solvation, and hydrophobic gating absent in its paralogs.Communications chemistry · 2026Article
- Quercetin Increases Expression of Membrane-TRAIL in Glioblastoma Cells Resulting in Apoptosis.Cancers · 2025Article
- Detection of p53 aggregates in plasma of glioma patients.Communications medicine · 2025Article
- Oncogenic p53 triggers amyloid aggregation of p63 and p73 liquid droplets.Communications chemistry · 2024Article
- IGF2BP3 promotes mRNA degradation through internal mNature communications · 2024Article
- Multiscale simulations reveal the driving forces of p53C phase separation accelerated by oncogenic mutations.Chemical science · 2024Article
- Enhancing Therapeutic Approaches in Glioblastoma with Pro-Oxidant Treatments and Synergistic Combinations: In Vitro Experience of Doxorubicin and Photodynamic Therapy.International journal of molecular sciences · 2024Article
- Unlocking the Gateway: The Spatio-Temporal Dynamics of the p53 Family Driven by the Nuclear Pores and Its Implication for the Therapeutic Approach in Cancer.International journal of molecular sciences · 2024Review
- Physiology and pharmacological targeting of phase separation.Journal of biomedical science · 2024Review
- Autophagy-associated biomarkers ULK2, UVRAG, and miRNAs miR-21, miR-126, and miR-374: Prognostic significance in glioma patients.PloS one · 2024Article
- Doxorubicin catalyses self-assembly of p53 by phase separation.Current research in structural biology · 2024Article
- Amyloids and brain cancer: molecular linkages and crossovers.Bioscience reports · 2023Review
- Protein nanocondensates: the next frontier.Biophysical reviews · 2023Review
- Molecular targeted therapy: A new avenue in glioblastoma treatment.Oncology letters · 2023Review
- TP53-PTEN-NF1 depletion in human brain organoids produces a glioma phenotypeFrontiers in oncology · 2023Article
- PRIMA-1 inhibits Y220C p53 amyloid aggregation and synergizes with cisplatin in hepatocellular carcinoma.Frontiers in molecular biosciences · 2023Article
- Transition of amyloid/mutant p53 from tumor suppressor to an oncogene and therapeutic approaches to ameliorate metastasis and cancer stemness.Cancer cell international · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor-associated p53 mutations endow cells with malignant phenotypes, including chemoresistance. Amyloid-like oligomers of mutant p53 transform this tumor suppressor into an oncogene. However, the composition and distribution of mutant p53 oligomers are unknown and the mechanism involved in the conversion is sparse. Here, we report accumulation of a p53 mutant within amyloid-like p53 oligomers in glioblastoma-derived cells presenting a chemoresistant gain-of-function phenotype. Statistical analysis from fluorescence fluctuation spectroscopy, pressure-induced measurements, and thioflavin T kinetics demonstrates the distribution of oligomers larger than the active tetrameric form of p53 in the nuclei of living cells and the destabilization of native-drifted p53 species that become amyloid. Collectively, these results provide insights into the role of amyloid-like mutant p53 oligomers in the chemoresistance phenotype of malignant and invasive brain tumors and shed light on therapeutic options to avert cancer.
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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.