ReviewCold Spring Harbor perspectives in medicine2016
The Role of the p53 Protein in Stem-Cell Biology and Epigenetic Regulation.
Review in Cold Spring Harbor perspectives in medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Is Hormone Replacement Therapy a Risk Factor or a Therapeutic Option for Alzheimer's Disease?International journal of molecular sciences · 2023Pooled it
- Why are Some Tissues More Vulnerable? Revisiting Tissue Specificity in Hereditary Cancer Syndromes.Molecular diagnosis & therapy · 2026Review
- p53 regulates the expression of histone modifiers to restrict stemness and maintain differentiated luminal identity in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Comprehensive secretome profiling and CRISPR screen identifies SFRP1 as a key inhibitor of epidermal progenitor proliferation.Cell death & disease · 2025Article
- Exploring the potential of machine learning in gastric cancer: prognostic biomarkers, subtyping, and stratification.BMC cancer · 2025Article
- The Original Mouse Models of Glioblastoma: Analysis of Pathophysiological Characteristics of Transplanted Tumor Tissue.Sovremennye tekhnologii v meditsine · 2025Article
- Ferroptosis in radiation-induced brain injury: roles and clinical implications.Biomedical engineering online · 2024Review
- The long and winding road of reprogramming-induced rejuvenation.Nature communications · 2024Review
- The AP-2 complex interacts with γ-TuRC and regulates the proliferative capacity of neural progenitors.Life science alliance · 2024Article
- Article
- Simplified Synthesis of Renieramycin T Derivatives to Target Cancer Stem Cells via β-Catenin Proteasomal Degradation in Human Lung Cancer.Marine drugs · 2023Article
- Article
- Review
- Transcriptome analysis reveals synergistic modulation of E-cadherin/N-cadherin in hMSC aggregates chondrogenesis.Genes & genomics · 2023Article
- Regulation of male germline transmission patterns by the Trp53-Cdkn1a pathway.Stem cell reports · 2022Article
- Impact of the interplay between stemness features, p53 and pol iota on replication pathway choices.Nucleic acids research · 2021Article
- Identification of DNA repair-related genes predicting pathogenesis and prognosis for liver cancer.Cancer cell international · 2021Article
- Small-cell lung cancer.Nature reviews. Disease primers · 2021Review
- The Interplay Between Tumor Suppressor p53 and Hypoxia Signaling Pathways in Cancer.Frontiers in cell and developmental biology · 2021Review
- Mutant p53 as an Antigen in Cancer Immunotherapy.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
The p53 protein plays a passive and an active role in stem cells. The transcriptional activities of p53 for cell-cycle arrest and DNA repair are largely turned off in stem cells, but there is some indication that long-term stem-cell viability may require other p53-regulated functions. When p53 is activated in stem cells, it stops cell division and promotes the commitment to a differentiation pathway and the formation of progenitor cells. In the absence of any p53 activity, stem-cell replication continues and mistakes in the normal epigenetic pathway occur at a higher probability. In the presence of a functionally active p53 protein, epigenetic stability is enforced and stem-cell replication is regulated by commitment to differentiation. Over a lifetime of an organism, stem-cell clones compete in a tissue niche for Darwinian replicative advantages and in doing so accumulate mutations that permit stem-cell replication. Mutations in the p53 gene give stem cells this advantage, increase the clonal stem-cell population, and lower the age at which cancers can occur. Li-Fraumeni patients that inherit p53 mutations develop tumors in a tissue-type-specific fashion at younger ages. Throughout the life of a Li-Fraumeni patient, the tumor types that arise occur in tissues where stem cells are active and cell division is most rapid. Thus, p53 mutations that are inherited or occur during developmental life act in stem cells of the mesenchymal and epithelial lineages, whereas p53 mutations that occur in progenitor or differentiated (somatic) cells later in life function in tissues of endodermal origins, indicating that p53 may function differently in different developmental lineages.
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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.