ReviewNature genetics2020
The critical roles of somatic mutations and environmental tumor-promoting agents in cancer risk.
Review in Nature genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
83 citing papers in PubMed, 157 citations in OpenAlex.
- A phase 2 study of spartalizumab (PDR001) among patients with recurrent or metastatic esophageal squamous cell carcinoma (KCSG HN18-17, K-MASTER project 12).Oncoimmunology · 2024Trial
- Intrinsic anti-tumorigenic properties of the skin epithelium promote cancer resistance in naked mole-rats.iScience · 2026Article
- Review
- Chemically induced skin tumors arise from long-lived stem cells of the upper hair follicle.Science (New York, N.Y.) · 2026Article
- Genome-scale molecular profiling from routine histopathology with a multimodal pathology foundation model.Research square · 2026Article
- Hallmarks of lung cancer driven by inhalable particulate matter: From cell-intrinsic oncogenic traits to microenvironment remodeling.Innovation (Cambridge (Mass.)) · 2026Review
- Effects of ethanol and acetaldehyde on multi-organ genomic mutation landscapes.Cell biology and toxicology · 2026Article
- A Critical Perspective on the Role of Thirdhand Smoke in Tumorigenesis: Initiator or Promoter.Environment & health (Washington, D.C.) · 2026Review
- What sets the mutation rate of a cell type in an animal species?PLoS biology · 2026Article
- Janus Nanoparticles in Doxorubicin Delivery: A New Frontier in Targeted Cancer Treatment.Materials (Basel, Switzerland) · 2026Review
- Review
- How somatic evolution affects health.Nature ecology & evolution · 2026Article
- A signature-agnostic test for differences between tumor mutation spectra reveals carcinogen and ancestry effects.Communications biology · 2026Article
- Rethinking the microenvironment's role in chemical-induced malignancy.Toxicological sciences : an official journal of the Society of Toxicology · 2026Review
- Pancreatic cancer: molecular pathogenesis and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Bile acids enrichment fuel tumor aerobic glycolysis and immune evasion via stabilizing FXR-RARα.Frontiers in immunology · 2026Article
- What sets the mutation rate of a cell type in an animal species?bioRxiv : the preprint server for biology · 2025Article
- Somatic mutation and selection at population scale.Nature · 2025Article
- Article
- Article
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Cancer is driven by genomic mutations in 'cancer driver' genes, which have essential roles in tumor development. These mutations may be caused by exposure to mutagens in the environment or by endogenous DNA-replication errors in tissue stem cells. Recent observations of abundant mutations, including cancer driver mutations, in histologically normal human tissues suggest that mutations alone are not sufficient for tumor development, thus prompting the question of how single mutant cells give rise to neoplasia. In a concept supported by decades-old data from mouse tumor models, non-mutagenic tumor-promoting agents have been posited to activate the proliferation of dormant mutated cells, thus generating actively growing lesions, with the promotion stage as the rate-limiting step in tumor formation. Non-mutagenic promoting agents, either endogenous or environmental, may therefore have a more important role in human cancer etiology than previously thought.
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What OpenQuestion holds
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.