ArticleNature genetics2020
Spatial competition shapes the dynamic mutational landscape of normal esophageal epithelium.
Article in Nature genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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Who cites it
96 citing papers in PubMed, 166 citations in OpenAlex.
- Epigenetic silencingCancer biology & therapy · 2026Article
- Cancer treatment alters mutant selection in normal esophagus.Nature genetics · 2026Article
- Prognostic significance of positive margin-informed tumor status in esophageal squamous cell carcinoma using next-generation sequencing.The oncologist · 2026Article
- Context-dependent selection sculpts mutational landscapes in the normal lung.Research square · 2026Article
- Spatiotemporal Transcriptomic Dissection Uncovers Age-Dependent Deceleration of Esophageal Cell Differentiation.bioRxiv : the preprint server for biology · 2026Article
- Article
- Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026Review
- Genotype-to-Phenotype Mapping of Somatic Clonal Mosaicism via Single-Cell Co-Capture of DNA Mutations and mRNA Transcripts.Cancer discovery · 2026Article
- Mitochondrial heteroplasmy is a risk factor for the development of chronic lymphocytic leukemia.Nature communications · 2026Article
- The dynamics of mutational selection in cutaneous squamous carcinogenesis.Communications biology · 2026Article
- Severity of effect considerations regarding the use of mutation as a toxicological endpoint for risk assessment: A report from the 8th International Workshop on Genotoxicity Testing (IWGT).Environmental and molecular mutagenesis · 2025Review
- Lifting regenerative barriers promotes epithelial cell fate plasticity supporting lineage conversion.Nature communications · 2025Article
- Large-scale single-cell phylogenetic mapping of clonal evolution in the human aging esophagus.bioRxiv : the preprint server for biology · 2025Article
- Age distinguishes selection from causation in cancer genomes.bioRxiv : the preprint server for biology · 2025Article
- Epithelial competition determines gene therapy potential to suppress Fanconi Anemia oral cancer risk.PLoS computational biology · 2025Article
- Cell sorting based on single nucleotide variation enables characterization of mutation-dependent transcriptome and chromatin states.Nucleic acids research · 2025Article
- Understanding the impact of mitochondrial DNA mutations on aging and carcinogenesis (Review).International journal of molecular medicine · 2025Review
- Aberrant Notch-signaling promotes tumor angiogenesis in esophageal squamous-cell carcinoma.Signal transduction and targeted therapy · 2025Article
- Epithelial competition determines gene therapy potential to suppress Fanconi Anemia oral cancer risk.bioRxiv : the preprint server for biology · 2025Article
- EarlybioRxiv : the preprint server for biology · 2025Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
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- Commented on byClone conflict.2020
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
During aging, progenitor cells acquire mutations, which may generate clones that colonize the surrounding tissue. By middle age, normal human tissues, including the esophageal epithelium (EE), become a patchwork of mutant clones. Despite their relevance for understanding aging and cancer, the processes that underpin mutational selection in normal tissues remain poorly understood. Here, we investigated this issue in the esophageal epithelium of mutagen-treated mice. Deep sequencing identified numerous mutant clones with multiple genes under positive selection, including Notch1, Notch2 and Trp53, which are also selected in human esophageal epithelium. Transgenic lineage tracing revealed strong clonal competition that evolved over time. Clone dynamics were consistent with a simple model in which the proliferative advantage conferred by positively selected mutations depends on the nature of the neighboring cells. When clones with similar competitive fitness collide, mutant cell fate reverts towards homeostasis, a constraint that explains how selection operates in normal-appearing epithelium.
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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.