Evidence map›Paper›PMID 21769933›Full record

ArticleGenetic epidemiology2011

A risk prediction algorithm based on family history and common genetic variants: application to prostate cancer with potential clinical impact.

Robert J Macinnis, Antonis C Antoniou, Rosalind A Eeles, Gianluca Severi, Ali Amin Al Olama, Lesley McGuffog, Zsofia Kote-Jarai, Michelle Guy, Lynne T O'Brien, Amanda L Hall and 14 more

Abstract read
In one paragraph

Article in Genetic epidemiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 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

50 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Multigene panels in prostate cancer risk assessment: a systematic review.Genetics in medicine : official journal of the American College of Medical Genetics · 2016
    Pooled it
  3. CanRisk-Prostate: A Comprehensive, Externally Validated Risk Model for the Prediction of Future Prostate Cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. A Review of Prostate Cancer Genome-Wide Association Studies (GWAS).Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018
    Review
  15. Observational
  16. Review
  17. Cancer management and research · 2018
    Article
  18. Article
  19. Prediction of Breast and Prostate Cancer Risks in Male BRCA1 and BRCA2 Mutation Carriers Using Polygenic Risk Scores.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2017
    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

24 authors.

Robert J MacinnisCentre for Cancer Genetic Epidemiology, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom.
Antonis C Antoniou
Rosalind A Eeles
Gianluca Severi
Ali Amin Al Olama
Lesley McGuffog
Zsofia Kote-Jarai
Michelle Guy
Lynne T O'Brien
Amanda L Hall
Rosemary A Wilkinson
Emma Sawyer
Audrey T Ardern-Jones
David P Dearnaley
Alan Horwich
Vincent S Khoo
Christopher C Parker
Robert A Huddart
Nicholas Van As
Margaret R McCredie
Dallas R English
Graham G Giles
John L Hopper
Douglas F Easton

Funding

Prostate Cancer Susceptibility: The ICPCG StudyU01CA089600 · NCI · MAYO CLINIC ROCHESTER · PI THIBODEAU, STEPHEN NORMAN · 2002 to 2016
$27.3M
Cancer Research UK 10118Cancer Research UK 10588Cancer Research UK 11022Cancer Research UK 11174Cancer Research UK C1287/A10118Cancer Research UK C5047/A3354NCI NIH HHS U01 CA089600NCI NIH HHS U01 CA89600
6 · The paper itself

Abstract

Genome wide association studies have identified several single nucleotide polymorphisms (SNPs) that are independently associated with small increments in risk of prostate cancer, opening up the possibility for using such variants in risk prediction. Using segregation analysis of population-based samples of 4,390 families of prostate cancer patients from the UK and Australia, and assuming all familial aggregation has genetic causes, we previously found that the best model for the genetic susceptibility to prostate cancer was a mixed model of inheritance that included both a recessive major gene component and a polygenic component (P) that represents the effect of a large number of genetic variants each of small effect, where . Based on published studies of 26 SNPs that are currently known to be associated with prostate cancer, we have extended our model to incorporate these SNPs by decomposing the polygenic component into two parts: a polygenic component due to the known susceptibility SNPs, , and the residual polygenic component due to the postulated but as yet unknown genetic variants, . The resulting algorithm can be used for predicting the probability of developing prostate cancer in the future based on both SNP profiles and explicit family history information. This approach can be applied to other diseases for which population-based family data and established risk variants exist.

Indexed as

Genome-Wide Association StudyAdultAgedAlgorithmsAustraliaGenetic VariationHumansMaleMiddle AgedModels, GeneticModels, StatisticalMolecular EpidemiologyPolymorphism, Single NucleotideProbabilityProstatic NeoplasmsRisk

Identifiers

PMID21769933
PMCPMC3950816

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Registered trials

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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.