ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2015
A metabolic perspective of Peto's paradox and 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 23 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.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Fraternal cooperation of hierarchical cancer parallels metazoan multicellularity and eusociality.Biological reviews of the Cambridge Philosophical Society · 2026Review
- Immunometabolic Gatekeeping: Reconciling Peto's & the T-cell Infiltration Prognostic Paradox.ArXiv · 2025Article
- Trans-Scale Insights into Variability in Radiation Cancer Risk Across Tissues, Individuals, and Species.Biology · 2025Review
- Limited cell-autonomous anticancer mechanisms in long-lived bats.Nature communications · 2025Article
- The hippo pathway: a molecular bridge between environmental cues and pace of life.BMC ecology and evolution · 2025Review
- When Do Tumours Develop? Neoplastic Processes Across Different Timescales: Age, Season and Round the Circadian Clock.Evolutionary applications · 2024Review
- 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
- White Paper: An Integrated Perspective on the Causes of Hypometric Metabolic Scaling in Animals.Integrative and comparative biology · 2022Article
- Cancer suppression and the evolution of multiple retrogene copies of TP53 in elephants: A re-evaluation.Evolutionary applications · 2022Article
- A novel perspective suggesting high sustained energy expenditure may be net protective against cancer.Evolution, medicine, and public health · 2022Article
- Low Cancer Incidence in Naked Mole-Rats May Be Related to Their Inability to Express the Warburg Effect.Frontiers in physiology · 2022Article
- A phylogenetic review of cancer resistance highlights evolutionary solutions to Peto's Paradox.Genetics and molecular biology · 2022Article
- What Animal Cancers teach us about Human Biology.Theranostics · 2021Review
- Resolving Peto's paradox: Modeling the potential effects of size-related metabolic changes, and of the evolution of immune policing and cancer suppression.Evolutionary applications · 2020Article
- Large Viable Fat Nodules, Months Post-Transfer, inside Radiated Breast Implant Pocket: A Case Report.Plastic and reconstructive surgery. Global open · 2020Article
- Article
- A Metabolism Toolbox for CAR T Therapy.Frontiers in oncology · 2019Review
- Aging, Metabolism, and Cancer Development: from Peto's Paradox to the Warburg Effect.Aging and disease · 2017Review
- Importance of metabolic rate to the relationship between the number of genes in a functional category and body size in Peto's paradox for cancer.Royal Society open science · 2016Article
- Evolutionary constraints over microsatellite abundance in larger mammals as a potential mechanism against carcinogenic burden.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The frequency of cancer is postulated to be proportional to the number of cells an animal possesses, as each cell is similarly exposed to mutagens with every cell division. Larger animals result from more cell divisions with more mutagenic exposure, and hence are expected to have higher frequencies of cancer. Yet, as stipulated by Peto's paradox, larger animals do not have the higher rates of cancers seen in smaller animals despite the significant differences in cell numbers and a longer lifetime that would expose larger animals to more mutagens. The rates of cancer appear to be inversely proportional to animal body size, which scales inversely with specific metabolic rates of mammals. Studies over the past 20 years have linked oncogenes and tumour suppressors to alterations in cancer metabolism, and conversely, mutations in metabolic genes have been documented to trigger tumorigenesis. The by-products and intermediates of metabolism, such as reactive oxygen species, oxoglutarate, citrate and acetate, all have the potential to mutate and alter the genome or epigenome. On the basis of these general observations, it is proposed that metabolic rates correlate with mutagenic rates, which are higher in small animals and give the mechanistic basis for Peto's paradox. The observations discussed in this overview collectively indicate that specific metabolic rate varies inversely with body size, which seems to support the hypothesis that metabolism drives tumorigenesis and accounts for Peto's paradox.
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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.