Evidence map›Paper›PMID 23396885›Full record

ArticleEvolutionary applications2013

Evolutionary foundations for cancer biology.

C Athena Aktipis, Randolph M Nesse

Erratum issuedOpen access · goldAbstract 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. An erratum has been issued. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
8.2field-weighted citation impact, top 2% of its field
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

94 citing papers in PubMed, 203 citations in OpenAlex.

  1. Article
  2. Studying adaptation at the invisible scale.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Review
  4. Article
  5. Epitranscriptomic sculpting: the role of mMedical oncology (Northwood, London, England) · 2025
    Review
  6. Article
  7. Review
  8. The Elephant and the Spandrel.Evolution, medicine, and public health · 2025
    Article
  9. De novo evolution of transmissible tumours in hydra.Proceedings. Biological sciences · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Life history traits and cancer prevalence in birds.Evolution, medicine, and public health · 2024
    Article
  14. The need for evolutionary theory in cancer research.European journal of epidemiology · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

34 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

C Athena AktipisCenter for Evolution and Cancer, University of California San Francisco, CA, USA ; Department of Psychology, Arizona State University Tempe, AZ, USA.
Randolph M Nesse
University of California, San Francisco · USUniversity of Michigan–Ann Arbor · US

Funding

Application of Evolutionary Principles to Maintain Cancer Control (PQ21)R01CA170595 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI GATENBY, ROBERT A · 2012 to 2015
$2.1M
Modeling causes and consequences of the evolution of cell motility in neoplasmsF32CA144331 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI AKTIPIS, CHRISTINA ATHENA · 2010 to 2012
$159k
NCI NIH HHS F32 CA144331NCI NIH HHS R01 CA170595
6 · The paper itself

Abstract

New applications of evolutionary biology are transforming our understanding of cancer. The articles in this special issue provide many specific examples, such as microorganisms inducing cancers, the significance of within-tumor heterogeneity, and the possibility that lower dose chemotherapy may sometimes promote longer survival. Underlying these specific advances is a large-scale transformation, as cancer research incorporates evolutionary methods into its toolkit, and asks new evolutionary questions about why we are vulnerable to cancer. Evolution explains why cancer exists at all, how neoplasms grow, why cancer is remarkably rare, and why it occurs despite powerful cancer suppression mechanisms. Cancer exists because of somatic selection; mutations in somatic cells result in some dividing faster than others, in some cases generating neoplasms. Neoplasms grow, or do not, in complex cellular ecosystems. Cancer is relatively rare because of natural selection; our genomes were derived disproportionally from individuals with effective mechanisms for suppressing cancer. Cancer occurs nonetheless for the same six evolutionary reasons that explain why we remain vulnerable to other diseases. These four principles-cancers evolve by somatic selection, neoplasms grow in complex ecosystems, natural selection has shaped powerful cancer defenses, and the limitations of those defenses have evolutionary explanations-provide a foundation for understanding, preventing, and treating cancer.

Indexed as

darwinianecologicalevolutionary medicinemismatchneoplasticvulnerability

Identifiers

PMID23396885
PMCPMC3567479
OpenAlexW2100124680

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.