ArticleCell stem cell2019
Outcompeting p53-Mutant Cells in the Normal Esophagus by Redox Manipulation.
Article in Cell stem cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.
- A meta-analysis identifies driver genes and characterizes the molecular epidemiology of colorectal cancer.Scientific reports · 2026Pooled it
- Cancer treatment alters mutant selection in normal esophagus.Nature genetics · 2026Article
- Dual contributions of Xrp1 to genome integrity through the DNA damage response and cell competition.PLoS genetics · 2026Article
- The Dynamic Alliance of p53 and Metabolism in the Tumor Microenvironment Shapes Tumor Evolution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Asymmetric division sustains stem cell heterogeneity in the Drosophila testicular niche.Communications biology · 2026Article
- Review
- Comparative Transcriptomics Reveals a Dual Role of the Epidermal Differentiation Complex in the Skin and the Oesophagus.Experimental dermatology · 2025Article
- Lifting regenerative barriers promotes epithelial cell fate plasticity supporting lineage conversion.Nature communications · 2025Article
- Cell Death, Compensatory Proliferation, and Cell Competition.Annual review of genetics · 2025Review
- Ovarian tumor cells gain competitive advantage by actively reducing the cellular fitness of microenvironment cells.Nature biotechnology · 2025Article
- Mechanisms of cellular fitness and cell competition: Towards an integrated view.Current opinion in cell biology · 2025Review
- Article
- Review
- Langerhans cell histiocytosis in children: the value of ultrasound in diagnosis and follow-up.BMC medical imaging · 2025Article
- Asymmetric stem cell division maintains genetic heterogeneity of tissue cells.bioRxiv : the preprint server for biology · 2024Article
- Organismal metabolism regulates the expansion of oncogenic PIK3CA mutant clones in normal esophagus.Nature genetics · 2024Article
- Non-genetic differences underlie variability in proliferation among esophageal epithelial clones.PLoS computational biology · 2024Article
- Self-sustaining long-term 3D epithelioid cultures reveal drivers of clonal expansion in esophageal epithelium.Nature genetics · 2024Article
- BNIP3-mediated mitophagy boosts the competitive growth of Lenvatinib-resistant cells via energy metabolism reprogramming in HCC.Cell death & disease · 2024Article
- Tumor initiation and early tumorigenesis: molecular mechanisms and interventional targets.Signal transduction and targeted therapy · 2024Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
As humans age, normal tissues, such as the esophageal epithelium, become a patchwork of mutant clones. Some mutations are under positive selection, conferring a competitive advantage over wild-type cells. We speculated that altering the selective pressure on mutant cell populations may cause them to expand or contract. We tested this hypothesis by examining the effect of oxidative stress from low-dose ionizing radiation (LDIR) on wild-type and p53 mutant cells in the transgenic mouse esophagus. We found that LDIR drives wild-type cells to stop proliferating and differentiate. p53 mutant cells are insensitive to LDIR and outcompete wild-type cells following exposure. Remarkably, combining antioxidant treatment and LDIR reverses this effect, promoting wild-type cell proliferation and p53 mutant differentiation, reducing the p53 mutant population. Thus, p53-mutant cells can be depleted from the normal esophagus by redox manipulation, showing that external interventions may be used to alter the mutational landscape of an aging tissue.
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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.