Evidence map›Paper›PMID 26091828›Full record

ReviewCancer discovery2015

APOBEC Enzymes: Mutagenic Fuel for Cancer Evolution and Heterogeneity.

Charles Swanton, Nicholas McGranahan, Gabriel J Starrett, Reuben S Harris

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 318 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
318citing papers in PubMed, 1 pooled it
15.1field-weighted citation impact, top 1% 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

318 citing papers in PubMed, 1 synthesis or guideline pooled it, 503 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Evolution ofInternational journal of molecular sciences · 2026
    Review
  9. Review
  10. Journal of virology · 2026
    Article
  11. Article
  12. Article
  13. HAMMER: Hairpin-based APOBEC3A-mediated mRNA editing reporter.bioRxiv : the preprint server for biology · 2026
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

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

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

4 authors at 1 institution in 1 country.

Charles SwantonThe Francis Crick Institute, London, United Kingdom. UCL Cancer Institute, CRUK Lung Cancer Centre of Excellence, London, United Kingdom. charles.swanton@crick.ac.uk rsh@umn.edu.
Nicholas McGranahanThe Francis Crick Institute, London, United Kingdom. Centre for Mathematics & Physics in the Life Sciences & Experimental Biology (CoMPLEX), University College London, London, United Kingdom.
Gabriel J StarrettDepartment of Biochemistry, Molecular Biology and Biophysics, Institute for Molecular Virology, and Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota.
Reuben S HarrisDepartment of Biochemistry, Molecular Biology and Biophysics, Institute for Molecular Virology, and Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota. charles.swanton@crick.ac.uk rsh@umn.edu.
The Francis Crick Institute · GB

Funding

Cancer Research UK 17786Cancer Research UK 19310Cancer Research UK A11590Cancer Research UK A17786Cancer Research UK A19310European Research Council 617844
6 · The paper itself

Abstract

unlabelledDeep sequencing technologies are revealing the complexities of cancer evolution, casting light on mutational processes fueling tumor adaptation, immune escape, and treatment resistance. Understanding mechanisms driving cancer diversity is a critical step toward developing strategies to attenuate tumor evolution and adaptation. One emerging mechanism fueling tumor diversity and subclonal evolution is genomic DNA cytosine deamination catalyzed by APOBEC3B and at least one other APOBEC family member. Deregulation of APOBEC3 enzymes causes a general mutator phenotype that manifests as diverse and heterogeneous tumor subclones. Here, we summarize knowledge of the APOBEC DNA deaminase family in cancer, and their role as driving forces for intratumor heterogeneity and a therapeutic target to limit tumor adaptation. SIGNIFICANCE: APOBEC mutational signatures may be enriched in tumor subclones, suggesting APOBEC cytosine deaminases fuel subclonal expansions and intratumor heterogeneity. APOBEC family members might represent a new class of drug target aimed at limiting tumor evolution, adaptation, and drug resistance.

Indexed as

MutationAPOBEC DeaminasesCytidine DeaminaseCytosineCytosine DeaminaseDeaminationEvolution, MolecularGenetic HeterogeneityHumansNeoplasmsAPOBEC3 proteins, humanAPOBEC DeaminasesCytidine DeaminaseCytosineCytosine Deaminase

Identifiers

PMID26091828
PMCPMC4497973
OpenAlexW1842792112

What OpenQuestion holds

Textmetadata
LicenceTDM
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.