ArticleOncotarget2015
Mutant p53 accumulates in cycling and proliferating cells in the normal tissues of p53 R172H mutant mice.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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
13 citing papers in PubMed, 25 citations in OpenAlex.
- Augmenting interferon-β and anti-PD-L1 antibody bolsters non-ablative radiotherapy to leverage potent abscopal effect in metastatic cancers.Frontiers in immunology · 2026Article
- The guardian of the genome meets immunotherapy: p53-based strategies.Frontiers in immunology · 2026Review
- Lymph node myeloid sarcoma with TP53‑associated myelodysplastic syndrome: A case report.Oncology letters · 2024Article
- Proteasome inhibitor bortezomib stabilizes and activates p53 in hematopoietic stem/progenitors and double-negative T cells in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- p53 mutation in normal esophagus promotes multiple stages of carcinogenesis but is constrained by clonal competition.Nature communications · 2022Article
- The Common GermlineCancer research · 2021Article
- Inhibition of p53 DNA binding by a small molecule protects mice from radiation toxicity.Oncogene · 2020Article
- Mutant p53 in colon cancer.Journal of molecular cell biology · 2019Review
- Mutant p53 Sequestration of the MDM2 Acidic Domain Inhibits E3 Ligase Activity.Molecular and cellular biology · 2019Article
- The Potential Roles of the Apoptosis-Related Protein PDRG1 in Diapause Embryo Restarting of Artemia sinica.International journal of molecular sciences · 2018Article
- The hot-spot p53R172H mutant promotes formation of giant spermatogonia triggered by DNA damage.Oncogene · 2017Article
- Exploiting the p53 Pathway for Therapy.Cold Spring Harbor perspectives in medicine · 2017Review
- Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
The tumour suppressor p53 is regulated primarily at the protein level. In normal tissues its levels are maintained at a very low level by the action of specific E3 ligases and the ubiquitin proteosome pathway. The mutant p53 protein contributes to transformation, metastasis and drug resistance. High levels of mutant p53 can be found in tumours and the accumulation of mutant p53 has previously been reported in pathologically normal cells in human skin. We show for the first time that similarly elevated levels of mutant p53 can be detected in apparently normal cells in a mutant p53 knock-in mouse model. In fact, in the small intestine, mutant p53 spontaneously accumulates in a manner dependent on gene dosage and cell type. Mutant p53 protein is regulated similarly to wild type p53, which can accumulate rapidly after induction by ionising radiation or Mdm2 inhibitors, however, the clearance of mutant p53 protein is much slower than wild type p53. The accumulation of the protein in the murine small intestine is limited to the cycling, crypt base columnar cells and proliferative zone and is lost as the cells differentiate and exit the cell cycle. Loss of Mdm2 results in even higher levels of p53 expression but p53 is still restricted to proliferating cells in the small intestine. Therefore, the small intestine of these p53 mutant mice is an experimental system in which we can dissect the molecular pathways leading to p53 accumulation, which has important implications for cancer prevention and therapy.
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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.