Evidence map›Paper›PMID 28336671›Full record

ArticleScience (New York, N.Y.)2017

Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention.

Cristian Tomasetti, Lu Li, Bert Vogelstein

Registry-linked trialAbstract read
In one paragraph

Article in Science (New York, N.Y.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05419531 (Measuring the Incidence of Colorectal Cancer in Young Endurance Athletes), which is not on this map. Cited by 518 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
518citing papers in PubMed, 1 pooled it
–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.

NCT05419531 completednot on this mapstarted 2022, after this paper: background citation

Measuring the Incidence of Colorectal Cancer in Young Endurance Athletes

TypeobservationalSponsorInova Health Care ServicesRan2022 to 2025Enrolled94ConditionsColorectal CancerArmsprospective observational study - screening and follow up colonoscopy
3 · Its place in the literature

Who cites it

518 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Indirect genomic effects shape cancer risk across species.bioRxiv : the preprint server for biology · 2026
    Article
  12. Review
  13. Integrated Clinicogenomic Risk Modeling for Metachronous Second Primary Cancers.medRxiv : the preprint server for health sciences · 2026
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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458 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Cristian TomasettiDivision of Biostatistics and Bioinformatics, Department of Oncology, Sidney Kimmel Cancer Center, Johns Hopkins University School of Medicine, 550 North Broadway, Baltimore, MD 21205, USA. ctomasetti@jhu.edu vogelbe@jhmi.edu.ORCID 0000-0003-3277-4804
Lu LiDepartment of Biostatistics, Johns Hopkins Bloomberg School of Public Health, 615 North Wolfe Street, Baltimore, MD 21205, USA.ORCID 0000-0002-1920-4965
Bert VogelsteinLudwig Center and Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, 1650 Orleans Street, Baltimore, MD 21205, USA. ctomasetti@jhu.edu vogelbe@jhmi.edu.ORCID 0000-0003-0766-3854

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
Tumor Antigens for Individual Signatures and TherapyP50CA062924 · NCI · JOHNS HOPKINS UNIVERSITY · PI LENNON, ANNE MARIE · 1993 to 2022
$54.6M
MOLECULAR GENETIC ANALYSIS OF COLORECTAL CANCERR37CA043460 · NCI · JOHNS HOPKINS UNIVERSITY · PI VOGELSTEIN, BERT · 1997 to 2016
$7.4M
NCI NIH HHS P30 CA006973NCI NIH HHS P50 CA062924NCI NIH HHS R37 CA043460
6 · The paper itself

Abstract

Cancers are caused by mutations that may be inherited, induced by environmental factors, or result from DNA replication errors (R). We studied the relationship between the number of normal stem cell divisions and the risk of 17 cancer types in 69 countries throughout the world. The data revealed a strong correlation (median = 0.80) between cancer incidence and normal stem cell divisions in all countries, regardless of their environment. The major role of R mutations in cancer etiology was supported by an independent approach, based solely on cancer genome sequencing and epidemiological data, which suggested that R mutations are responsible for two-thirds of the mutations in human cancers. All of these results are consistent with epidemiological estimates of the fraction of cancers that can be prevented by changes in the environment. Moreover, they accentuate the importance of early detection and intervention to reduce deaths from the many cancers arising from unavoidable R mutations.

Indexed as

Cell DivisionAfricaAsiaCaribbean RegionDNA ReplicationFemaleGene-Environment InteractionHumansIncidenceLatin AmericaMaleMutationNeoplasmsNorth AmericaOceaniaPrimary Prevention

Identifiers

PMID28336671
PMCPMC5852673

What OpenQuestion holds

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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.