Evidence map›Paper›PMID 24296704›Full record

ReviewNature reviews. Urology2014

The genetic epidemiology of prostate cancer and its clinical implications.

Rosalind Eeles, Chee Goh, Elena Castro, Elizabeth Bancroft, Michelle Guy, Ali Amin Al Olama, Douglas Easton, Zsofia Kote-Jarai

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Urology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 8 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.

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

127 citing papers in PubMed, 8 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Pooled it
  8. Pooled it
  9. Trial
  10. Trial
  11. Article
  12. Cancer disparities: an extensive review.Ecancermedicalscience · 2026
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

67 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

8 authors.

Rosalind EelesOncogenetics Team, Division of Cancer Genetics and Epidemiology, The Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey SM2 5NG, UK.
Chee GohOncogenetics Team, Division of Cancer Genetics and Epidemiology, The Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey SM2 5NG, UK.
Elena CastroOncogenetics Team, Division of Cancer Genetics and Epidemiology, The Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey SM2 5NG, UK.
Elizabeth BancroftClinical Academic Cancer Genetics Unit, The Royal Marsden NHS Foundation Trust, Sutton, Surrey SM2 5PT, UK.
Michelle GuyOncogenetics Team, Division of Cancer Genetics and Epidemiology, The Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey SM2 5NG, UK.
Ali Amin Al OlamaCancer Research UK Centre for Cancer Genetic Epidemiology, Strangeways Laboratory, University of Cambridge, Cambridge CB1 8RN, UK.
Douglas EastonDepartments of Public Health & Primary Care and Oncology, Strangeways Laboratory, University of Cambridge, Cambridge CB1 8RN, UK.
Zsofia Kote-JaraiOncogenetics Team, Division of Cancer Genetics and Epidemiology, The Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey SM2 5NG, UK.

Funding

Epidemiological and Clinical Translational Studies Post Genome-Wide AssociationU19CA148537 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI EASTON, DOUGLAS FREDERICK, EELES, ROSALIND · 2010 to 2014
$10.4M
Cancer Research UK 13232Cancer Research UK 15007Cancer Research UK 16563Cancer Research UK C5047/A10692Cancer Research UK C5047/A13232NCI NIH HHS U19CA148537
6 · The paper itself

Abstract

Worldwide, familial and epidemiological studies have generated considerable evidence of an inherited component to prostate cancer. Indeed, rare highly penetrant genetic mutations have been implicated. Genome-wide association studies (GWAS) have also identified 76 susceptibility loci associated with prostate cancer risk, which occur commonly but are of low penetrance. However, these mutations interact multiplicatively, which can result in substantially increased risk. Currently, approximately 30% of the familial risk is due to such variants. Evaluating the functional aspects of these variants would contribute to our understanding of prostate cancer aetiology and would enable population risk stratification for screening. Furthermore, understanding the genetic risks of prostate cancer might inform predictions of treatment responses and toxicities, with the goal of personalized therapy. However, risk modelling and clinical translational research are needed before we can translate risk profiles generated from these variants into use in the clinical setting for targeted screening and treatment.

Indexed as

Genetic Predisposition to DiseaseGenome-Wide Association StudyGlobal HealthHumansMaleMolecular EpidemiologyMorbidityProstatic Neoplasms

Identifiers

What OpenQuestion holds

Textmetadata
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.