Evidence map›Paper›PMID 26068399›Full record

ArticleBritish journal of cancer2015

An analysis of the association between prostate cancer risk loci, PSA levels, disease aggressiveness and disease-specific mortality.

J Sullivan, R Kopp, K Stratton, C Manschreck, M Corines, R Rau-Murthy, J Hayes, A Lincon, A Ashraf, T Thomas and 10 more

Abstract read
In one paragraph

Article in British journal of cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing 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.

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

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

  1. Pooled it
  2. Article
  3. Article
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  5. Article
  6. Article
  7. Article
  8. Review
  9. SNPs at SMG7 Associated with Time from Biochemical Recurrence to Prostate Cancer Death.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2022
    Article
  10. Review
  11. Article
  12. Article
  13. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors.

J Sullivan1] Department of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA [2] Department of Surgery, Urology Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
R Kopp1] Department of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA [2] Department of Surgery, Urology Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
K Stratton1] Department of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA [2] Department of Surgery, Urology Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
C ManschreckDepartment of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
M CorinesDepartment of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
R Rau-MurthyDepartment of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
J HayesDepartment of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
A LinconDepartment of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
A AshrafDepartment of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
T ThomasDepartment of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
K SchraderDepartment of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
D GallagherDepartment of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
R HamiltonDepartment of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
H ScherDepartment of Medicine, Genitourinary Medical Oncology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
H LiljaDepartment of Surgery, Urology Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
P ScardinoDepartment of Surgery, Urology Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
J EasthamDepartment of Surgery, Urology Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
K OffitDepartment of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
J VijaiDepartment of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
R J Klein1] Department of Medicine, Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, NY, USA [2] Icahn Institute for Genomics and Multiscale Biology, Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Clinical and Translational Science CenterUL1TR000457 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IMPERATO-MCGINLEY, JULIANNE L · 2012 to 2016
$46.0M
Improving prostate cancer screening by integration of SNPs with blood biomarkersR01CA175491 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI KLEIN, ROBERT J. · 2013 to 2018
$2.8M
NCATS NIH HHS UL1 TR000457NCI NIH HHS P30 CA008748NCI NIH HHS R01 CA175491
6 · The paper itself

Abstract

backgroundGenome-wide association studies have identified multiple single-nucleotide polymorphsims (SNPs) associated with prostate cancer (PCa). Although these SNPs have been clearly associated with disease risk, their relationship with clinical outcomes is less clear. Our aim was to assess the frequency of known PCa susceptibility alleles within a single institution ascertainment and to correlate risk alleles with disease-specific outcomes.

methodsWe genotyped 1354 individuals treated for localised PCa between June 1988 and December 2007. Blood samples were prospectively collected and de-identified before being genotyped and matched to phenotypic data. We investigated associations between 61 SNPs and disease-specific end points using multivariable analysis and also determined if SNPs were associated with PSA at diagnosis.

resultsSeven SNPs showed associations on multivariable analysis (P<0.05), rs13385191 with both biochemical recurrence (BR) and castrate metastasis (CM), rs339331 (BR), rs1894292, rs17178655 and rs11067228 (CM), and rs11902236 and rs4857841 PCa-specific mortality. After applying a Bonferroni correction for number of SNPs (P<0.0008), the only persistent significant association was between rs17632542 (KLK3) and PSA levels at diagnosis (P=1.4 × 10(-5)).

conclusionsWe confirmed that rs17632542 in KLK3 is associated with PSA at diagnosis. No significant association was seen between loci and disease-specific end points when accounting for multiple testing. This provides further evidence that known PCa risk SNPs do not predict likelihood of disease progression.

Indexed as

Genetic Predisposition to DiseaseHumansMaleProstate-Specific AntigenProstatic NeoplasmsProstate-Specific Antigen

Identifiers

PMID26068399
PMCPMC4647539

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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.