Evidence map›Paper›PMID 23396800›Full record

ArticleEvolutionary applications2013

Peto's paradox revisited: theoretical evolutionary dynamics of cancer in wild populations.

Benjamin Roche, Kathleen Sprouffske, Hassan Hbid, Dorothée Missé, Frédéric Thomas

Abstract read
In one paragraph

Article in Evolutionary applications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed.

  1. Article
  2. Article
  3. Life history traits and cancer prevalence in birds.Evolution, medicine, and public health · 2024
    Article
  4. Life history and cancer in birds: clutch size predicts cancer.bioRxiv : the preprint server for biology · 2023
    Article
  5. Cell size, body size and Peto's paradox.BMC ecology and evolution · 2022
    Review
  6. The occurrence of cancer in vertebrates: a mini review.Journal of biological research (Thessalonike, Greece) · 2020
    Review
  7. Article
  8. Article
  9. Review
  10. The multiple facets of Peto's paradox: a life-history model for the evolution of cancer suppression.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    Article
  11. A metabolic perspective of Peto's paradox and cancer.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    Review
  12. Towards cancer-aware life-history modelling.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    Article
  13. Cancer susceptibility and reproductive trade-offs: a model of the evolution of cancer defences.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2015
    Article
  14. Review
  15. Article
  16. Article
  17. Evolutionary foundations for cancer biology.Evolutionary applications · 2013
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Benjamin RocheIRD, UMMISCO (UMI IRD/UPMC) Bondy, France ; CREEC, Université Montpellier 2 Montpellier, France.
Kathleen Sprouffske
Hassan Hbid
Dorothée Missé
Frédéric Thomas

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

If the occurrence of cancer is the result of a random lottery among cells, then body mass, a surrogate for cells number, should predict cancer incidence. Despite some support in humans, this assertion does not hold over the range of different natural animal species where cancer incidence is known. Explaining the so-called 'Peto's paradox' is likely to increase our understanding of how cancer defense mechanisms are shaped by natural selection. Here, we study how body mass may affect the evolutionary dynamics of tumor suppressor gene (TSG) inactivation and oncogene activation in natural animal species. We show that the rate of TSG inactivation should evolve to lower values along a gradient of body mass in a nonlinear manner, having a threshold beyond which benefits to adaptive traits cannot overcome their costs. We also show that oncogenes may be frequently activated within populations of large organisms. We then propose experimental settings that can be employed to identify protection mechanisms against cancer. We finally highlight fundamental species traits that natural selection should favor against carcinogenesis. We conclude on the necessity of comparing genomes between populations of a single species or genomes between species to better understand how evolution has molded protective mechanisms against cancer development and associated mortality.

Indexed as

biomedicinedisease biologyevolutionary medicineevolutionary theory

Identifiers

PMID23396800
PMCPMC3567476

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.