ArticlePhilosophical transactions of the Royal Society of London. Series B, Biological sciences2015
Peto's paradox and human cancers.
Article in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed, 65 citations in OpenAlex.
- Body height and the excess cancer risk in men.International journal of cancer · 2026Article
- Evolutionary Dynamics of Oncosuppression Under Selection Pressure.Life (Basel, Switzerland) · 2025Article
- Towards a more robust comparative oncology: a Bayesian reanalysis of Peto's paradox and discussion of comparative cancer risk studies in vertebrates.Royal Society open science · 2025Article
- Reply to Compton et al.: Paradoxical misunderstanding.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cancer Prevalence across Vertebrates.Cancer discovery · 2025Article
- Review
- Cell size, body size and Peto's paradox.BMC ecology and evolution · 2022Review
- Trade-off between reducing mutational accumulation and increasing commitment to differentiation determines tissue organization.Nature communications · 2022Article
- Increased risk of cancer in dogs and humans: a consequence of recent extension of lifespan beyond evolutionarily-determined limitations?Aging and cancer · 2022Article
- Identifying key questions in the ecology and evolution of cancer.Evolutionary applications · 2021Article
- Determining cancer risk: the evolutionary multistage model or total stem cell divisions?Proceedings. Biological sciences · 2020Article
- Comparative Oncology: New Insights into an Ancient Disease.iScience · 2020Review
- Differences in mutational processes and intra-tumour heterogeneity between organs: The local selective filter hypothesis.Evolution, medicine, and public health · 2019Review
- Size matters: height, cell number and a person's risk of cancer.Proceedings. Biological sciences · 2018Article
- Replicative cellular age distributions in compartmentalized tissues.Journal of the Royal Society, Interface · 2018Article
- Big Bang Tumor Growth and Clonal Evolution.Cold Spring Harbor perspectives in medicine · 2018Review
- All's well that ends well: why large species have short telomeres.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018Article
- An ecosystem framework for understanding and treating disease.Evolution, medicine, and public health · 2018Review
- Inequality in genetic cancer risk suggests bad genes rather than bad luck.Nature communications · 2017Article
- Racial disparities in patient survival and tumor mutation burden, and the association between tumor mutation burden and cancer incidence rate.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peto's paradox is the lack of the expected trend in cancer incidence as a function of body size and lifespan across species. The leading hypothesis to explain this pattern is natural selection for differential cancer prevention in larger, longer lived species. We evaluate whether a similar effect exists within species, specifically humans. We begin by reanalysing a recently published dataset to separate the effects of stem cell number and replication rate, and show that each has an independent effect on cancer risk. When considering the lifetime number of stem cell divisions in an extended dataset, and removing cases associated with other diseases or carcinogens, we find that lifetime cancer risk per tissue saturates at approximately 0.3-1.3% for the types considered. We further demonstrate that grouping by anatomical site explains most of the remaining variation. Our results indicate that cancer risk depends not only on the number of stem cell divisions but varies enormously (approx. 10 000 times) depending on anatomical site. We conclude that variation in risk of human cancer types is analogous to the paradoxical lack of variation in cancer incidence among animal species and may likewise be understood as a result of evolution by natural selection.
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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.