Evidence map›Paper›PMID 24753544›Full record

SynthesisCancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology2014

Genetic variation in prostate-specific antigen-detected prostate cancer and the effect of control selection on genetic association studies.

Duleeka W Knipe, David M Evans, John P Kemp, Rosalind Eeles, Douglas F Easton, Zsofia Kote-Jarai, Ali Amin Al Olama, Sara Benlloch, Jenny L Donovan, Freddie C Hamdy and 4 more

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Characterization of Genetic Etiologic Factors for Pediatric Acute Lymphoblastic Leukemia in Large Childhood Cancer Survivorship Cohorts.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2026
    Article
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  7. Article
  8. Article
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  10. Cancer Progress and Priorities: Prostate Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2020
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Genetic Association betweenFrontiers in physiology · 2017
    Article
  16. Review
  17. Prostate Cancer: Is It a Battle Lost to Age?Geriatrics (Basel, Switzerland) · 2016
    Review
  18. Article
  19. Article
  20. Article
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

14 authors at 8 institutions in 3 countries.

Duleeka W KnipeSchool of Social and Community Medicine, University of Bristol, Bristol, United Kingdom.
David M EvansSchool of Social and Community Medicine, University of Bristol, Bristol, United Kingdom.
John P KempSchool of Social and Community Medicine, University of Bristol, Bristol, United Kingdom.
Rosalind EelesThe Institute of Cancer Research, Sutton, Surrey, UK.
Douglas F EastonCancer Research UK Genetic Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Strangeways Laboratory, Cambridge, UK.
Zsofia Kote-JaraiThe Institute of Cancer Research, Sutton, Surrey, UK.
Ali Amin Al OlamaCancer Research UK Genetic Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Strangeways Laboratory, Cambridge, UK.
Sara BenllochCancer Research UK Genetic Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Strangeways Laboratory, Cambridge, UK.
Jenny L DonovanSchool of Social and Community Medicine, University of Bristol, Bristol, United Kingdom.
Freddie C HamdyNuffield Department of Surgery, University of Oxford, Oxford, United Kingdom.
David E NealThe Royal Marsden National Health Service Foundation Trust, Sutton, Surrey and London, UK.
George Davey Smith *School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom.
Mark Lathrop *Commissariat à l'Energie Atomique, Center National de Génotypage, Evry, France.
Richard M Martin *School of Social and Community Medicine, University of Bristol, Bristol, United Kingdom.
University of Bristol · GBUniversity of Cambridge · GBCancer Research UK · GBCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FRInstitute of Cancer Research · GBMRC Epidemiology Unit · GBNational Health Service · GBUniversity of Oxford · GB

Funding

Cancer Research UK 10118Cancer Research UK 11022Cancer Research UK 15007Cancer Research UK 16563Cancer Research UK 17528Cancer Research UK A10118Cancer Research UK A7357Cancer Research UK C1287/A10118Cancer Research UK C5047/A7357Cancer Research UK G0500966/75466Department of Health HTA_179Medical Research Council G0500966(75466)Medical Research Council G0900871Medical Research Council MC_UU_12013/1Medical Research Council MC_UU_12013/4Wellcome Trust 099874Wellcome Trust WT099874MA
6 · The paper itself

Abstract

backgroundOnly a minority of the genetic components of prostate cancer risk have been explained. Some observed associations of SNPs with prostate cancer might arise from associations of these SNPs with circulating prostate-specific antigen (PSA) because PSA values are used to select controls.

methodsWe undertook a genome-wide association study (GWAS) of screen-detected prostate cancer (ProtecT: 1,146 cases and 1,804 controls); meta-analyzed the results with those from the previously published UK Genetic Prostate Cancer Study (1,854 cases and 1,437 controls); investigated associations of SNPs with prostate cancer using either "low" (PSA < 0.5 ng/mL) or "high" (PSA ≥ 3 ng/mL, biopsy negative) PSA controls; and investigated associations of SNPs with PSA.

resultsThe ProtecT GWAS confirmed previously reported associations of prostate cancer at three loci: 10q11.23, 17q24.3, and 19q13.33. The meta-analysis confirmed associations of prostate cancer with SNPs near four previously identified loci (8q24.21,10q11.23, 17q24.3, and 19q13.33). When comparing prostate cancer cases with low PSA controls, alleles at genetic markers rs1512268, rs445114, rs10788160, rs11199874, rs17632542, rs266849, and rs2735839 were associated with an increased risk of prostate cancer, but the effect-estimates were attenuated to the null when using high PSA controls (Pheterogeneity in effect-estimates < 0.04). We found a novel inverse association of rs9311171-T with circulating PSA.

conclusionsDifferences in effect-estimates for prostate cancer observed when comparing low versus high PSA controls may be explained by associations of these SNPs with PSA. IMPACT: These findings highlight the need for inferences from genetic studies of prostate cancer risk to carefully consider the influence of control selection criteria.

Indexed as

AgedGenetic Association StudiesGenetic Predisposition to DiseaseGenotypeHumansMaleMiddle AgedPolymorphism, Single NucleotideProstate-Specific AntigenProstatic NeoplasmsProstate-Specific Antigen

Identifiers

PMID24753544
PMCPMC4082405
OpenAlexW2122594005

What OpenQuestion holds

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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.