ReviewCancer discovery2022
Somatic Mutation: What Shapes the Mutational Landscape of Normal Epithelia?
Review in Cancer discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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.
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
37 citing papers in PubMed, 34 citations in OpenAlex.
- Cancer treatment alters mutant selection in normal esophagus.Nature genetics · 2026Article
- Chemically induced skin tumors arise from long-lived stem cells of the upper hair follicle.Science (New York, N.Y.) · 2026Article
- Hallmarks of lung cancer driven by inhalable particulate matter: From cell-intrinsic oncogenic traits to microenvironment remodeling.Innovation (Cambridge (Mass.)) · 2026Review
- The role of cytotoxicity in the process of carcinogenesis.Archives of toxicology · 2026Article
- Context-dependent selection sculpts mutational landscapes in the normal lung.Research square · 2026Article
- Genetic Landscape of Oral Carcinoma Cuniculatum and its Histological Mimics.Head and neck pathology · 2026Article
- Article
- The dynamics of mutational selection in cutaneous squamous carcinogenesis.Communications biology · 2026Article
- Article
- Stem cell competition.Current topics in developmental biology · 2026Review
- Arid1a Deficiency Drives Aristolochic Acid-Induced Liver Tumorigenesis through Ctnnb1 Mutation and Defective Nucleotide Excision Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Early mutational events and clonal dynamics in normal crypts: implications for colorectal tumorigenesis.Human genomics · 2025Review
- Genetic evolution of keratinocytes to cutaneous squamous cell carcinoma.Nature communications · 2025Article
- Article
- Greater lung cancer polygenic risk score in higher air pollution areas linked to greater rate of lung adenocarcinoma: a single-centre study in East Asia.BMJ open respiratory research · 2025Article
- Modelling the ageing dependence of cancer evolutionary trajectories.Nature reviews. Cancer · 2025Review
- A Universal Duplex Sequencing Approach for Accurate Detection of Somatic Mutations.bioRxiv : the preprint server for biology · 2025Article
- Radiation effects research foundation-a view to the future.Carcinogenesis · 2025Article
- X-linked competition - implications for human development and disease.Nature reviews. Genetics · 2025Review
- CD103Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 3 countries.
Funding
Abstract
Epithelial stem cells accumulate mutations throughout life. Some of these mutants increase competitive fitness and may form clones that colonize the stem cell niche and persist to acquire further genome alterations. After a transient expansion, mutant stem cells must revert to homeostatic behavior so normal tissue architecture is maintained. Some positively selected mutants may promote cancer development, whereas others inhibit carcinogenesis. Factors that shape the mutational landscape include wild-type and mutant stem cell dynamics, competition for the niche, and environmental exposures. Understanding these processes may give new insight into the basis of cancer risk and opportunities for cancer prevention. SIGNIFICANCE: Recent advances in sequencing have found somatic mutations in all epithelial tissues studied to date. Here we review how the mutational landscape of normal epithelia is shaped by clonal competition within the stem cell niche combined with environmental exposures. Some of the selected mutant genes are oncogenic, whereas others may be inhibitory of transformation. Discoveries in this area leave many open questions, such as the definition of cancer driver genes, the mechanisms by which tissues constrain a high proportion of oncogenic mutant cells, and whether clonal fitness can be modulated to decrease cancer risk.
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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.