ArticleCommunications biology2019
Irradiation induces p53 loss of heterozygosity in breast cancer expressing mutant p53.
Article in Communications biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Review
- Glioma stem cells: drivers of tumor progression and recurrence.Stem cell research & therapy · 2025Review
- Mutant p53 upregulates HDAC6 to resist ER stress and facilitates Ku70 deacetylation, which prevents its degradation and mitigates DNA damage in colon cancer cells.Cell death discovery · 2025Article
- Impact of Proton Irradiation Depending on Breast Cancer Subtype in Patient-Derived Cell Lines.International journal of molecular sciences · 2024Article
- Suppression of HSF1 activity by wildtype p53 creates a driving force for p53 loss-of-heterozygosity.Nature communications · 2021Article
- Mutant p53 drives the loss of heterozygosity by the upregulation of Nek2 in breast cancer cells.Breast cancer research : BCR · 2020Article
- Attenuation of p53 mutant as an approach for treatment Her2-positive cancer.Cell death discovery · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in one allele of the TP53 gene in cancer early stages are frequently followed by the loss of the remaining wild-type allele (LOH) during tumor progression. However, the clinical impact of TP53 mutations and p53LOH, especially in the context of genotoxic modalities, remains unclear. Using MMTV;ErbB2 model carrying a heterozygous R172H p53 mutation, we report a previously unidentified oncogenic activity of mutant p53 (mutp53): the exacerbation of p53LOH after irradiation. We show that wild-type p53 allele is partially transcriptionally competent and enables the maintenance of the genomic integrity under normal conditions in mutp53 heterozygous cells. In heterozygous cells γ-irradiation promotes mutp53 stabilization, which suppresses DNA repair and the cell cycle checkpoint allowing cell cycle progression in the presence of inefficiently repaired DNA, consequently increases genomic instability leading to p53LOH. Hence, in mutp53 heterozygous cells, irradiation facilitates the selective pressure for p53LOH that enhances cancer cell fitness and provides the genetic plasticity for acquiring metastatic properties.
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Registered trials
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