ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2015
Peto's paradox and the hallmarks of cancer: constructing an evolutionary framework for understanding the incidence of cancer.
Review 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 26 papers.
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Who cites it
26 citing papers in PubMed.
- Of Barriers and Loops-How Evolution Limits Most Cancer Risks to Older Ages.Cancer discovery · 2026Review
- Assessment of knowledge, attitude and practice (KAP) regarding siddha medicines by veterinarians in Tamil Nadu: A cross-sectional observational study.Bioinformation · 2025Article
- The effect of body size and inbreeding on cancer mortality in breeds of the domestic dog: a test of the multi-stage model of carcinogenesis.Royal Society open science · 2024Article
- Quantifying substantial carcinogenesis of genetic and environmental factors from measurement error in the number of stem cell divisions.BMC cancer · 2022Article
- Immunotoxicity of nanomaterials in health and disease: Current challenges and emerging approaches for identifying immune modifiers in susceptible populations.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2022Review
- A phylogenetic review of cancer resistance highlights evolutionary solutions to Peto's Paradox.Genetics and molecular biology · 2022Article
- Positive selection and gene duplications in tumour suppressor genes reveal clues about how cetaceans resist cancer.Proceedings. Biological sciences · 2021Article
- Conservation of A-to-I RNA editing in bowhead whale and pig.PloS one · 2021Article
- Determining cancer risk: the evolutionary multistage model or total stem cell divisions?Proceedings. Biological sciences · 2020Article
- Dichotomous Impact of Myc on rRNA Gene Activation and Silencing in B Cell Lymphomagenesis.Cancers · 2020Article
- Comparative Oncology: New Insights into an Ancient Disease.iScience · 2020Review
- The three dimensions of somatic evolution: Integrating the role of genetic damage, life-history traits, and aging in carcinogenesis.Evolutionary applications · 2020Article
- Predation shapes the impact of cancer on population dynamics and the evolution of cancer resistance.Evolutionary applications · 2020Article
- Lifetime cancer prevalence and life history traits in mammals.Evolution, medicine, and public health · 2020Article
- Tumorigenesis as the Paradigm of Quasi-neutral Molecular Evolution.Molecular biology and evolution · 2019Article
- Review
- Estimating the number of genetic mutations (hits) required for carcinogenesis based on the distribution of somatic mutations.PLoS computational biology · 2019Article
- Size matters: height, cell number and a person's risk of cancer.Proceedings. Biological sciences · 2018Article
- From humans to hydra: patterns of cancer across the tree of life.Biological reviews of the Cambridge Philosophical Society · 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
Corrections and comments
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Authors and funding
2 authors.
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No grant is acknowledged in the PubMed record.
Abstract
An evolutionary perspective can help unify disparate observations and make testable predictions. We consider an evolutionary model in relation to two mechanistic frameworks of cancer biology: multistage carcinogenesis and the hallmarks of cancer. The multistage model predicts that cancer risk increases with body size and longevity; however, this is not observed across species (Peto's paradox), but the paradox is resolved by invoking the evolution of additional genetic mechanisms to suppress cancer in large, long-lived species. It is when cancer cells overcome these defence mechanisms that they exhibit the hallmarks of cancer, driving the ongoing evolution of these defences, which in turn is expected to create the differences observed in the genetics of cancer across species and tissues. To illustrate the utility of an evolutionary model we examined some recently published data linking stem-cell divisions and cancer incidence across a range of tissues and show why the original analysis was faulty, and demonstrate that the data are consistent with a multistage model varying from three to seven mutational hits across different tissues. Finally, we demonstrate how an evolutionary model can both define patterns of inherited (familial) cancer and explain the prevalence of cancer in post-reproductive years, including the dominance of epithelial cancers.
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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.