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Peto's paradox and human cancers.

Robert Noble1, Oliver Kaltz1, Michael E Hochberg2

  • 1Institut des Sciences de l'Evolution, Université de Montpellier, Place Eugène Bataillon, 34095 Montpellier Cedex 5, France.

Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
|June 10, 2015
PubMed
Summary
This summary is machine-generated.

Cancer risk in humans shows a pattern similar to Peto's paradox. Evolution by natural selection may explain why cancer risk varies greatly by anatomical site, not just stem cell divisions.

Keywords:
Peto's paradoxcancercarcinogenesisdiseasestem cells‘bad luck’ mutations

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Area of Science:

  • Evolutionary Biology
  • Cancer Research
  • Genetics

Background:

  • Peto's paradox describes the unexpected lack of correlation between body size/lifespan and cancer incidence across species.
  • The prevailing hypothesis suggests natural selection favors cancer prevention in larger, longer-lived animals.
  • This study investigates if similar evolutionary pressures influence cancer risk within species, specifically humans.

Purpose of the Study:

  • To determine if Peto's paradox, observed across species, is also applicable within humans.
  • To analyze the independent contributions of stem cell number and replication rate to cancer risk.
  • To explore the role of anatomical site in cancer risk variation.

Main Methods:

  • Reanalysis of existing cancer incidence datasets.
  • Separation of stem cell number and replication rate effects on cancer risk.
  • Analysis of lifetime stem cell divisions and cancer risk across different human tissues and anatomical sites.

Main Results:

  • Stem cell number and replication rate independently impact cancer risk.
  • Lifetime cancer risk per tissue saturates at approximately 0.3-1.3% after accounting for other factors.
  • Cancer risk varies significantly (up to 10,000-fold) by anatomical site, more so than by stem cell divisions alone.

Conclusions:

  • Human cancer risk variation mirrors Peto's paradox observed across species.
  • Natural selection likely drives differential cancer risk based on anatomical site and evolutionary pressures.
  • Cancer risk is influenced by both stem cell division rates and specific anatomical site adaptations.