Evidence map›Paper›PMID 33258481›Full record

ArticleThe Prostate2020

Validation of a prostate cancer polygenic risk score.

Mary H Black, Shuwei Li, Holly LaDuca, Min-Tzu Lo, Jefferey Chen, Robert Hoiness, Stephanie Gutierrez, Brigette Tippin-Davis, Hsiao-Mei Lu, Marta Gielzak and 7 more

Open access · hybridAbstract read
In one paragraph

Article in The Prostate, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

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  14. Race and prostate cancer: genomic landscape.Nature reviews. Urology · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 3 institutions in 1 country.

Mary H BlackAmbry Genetics, Aliso Viejo, California.
Shuwei LiAmbry Genetics, Aliso Viejo, California.ORCID 0000-0001-7176-1964
Holly LaDucaAmbry Genetics, Aliso Viejo, California.
Min-Tzu LoAmbry Genetics, Aliso Viejo, California.
Jefferey ChenAmbry Genetics, Aliso Viejo, California.
Robert HoinessAmbry Genetics, Aliso Viejo, California.
Stephanie GutierrezAmbry Genetics, Aliso Viejo, California.
Brigette Tippin-DavisAmbry Genetics, Aliso Viejo, California.
Hsiao-Mei LuAmbry Genetics, Aliso Viejo, California.
Marta GielzakDepartment of Urology, The James Buchanan Brady Urologic Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Kathleen WileyDepartment of Urology, The James Buchanan Brady Urologic Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Zhuqing ShiProgram for Personalized Cancer Care, NorthShore University Health System, Evanston, Illinois.ORCID 0000-0001-6321-950X
Jun WeiProgram for Personalized Cancer Care, NorthShore University Health System, Evanston, Illinois.
Siqun Lilly ZhengProgram for Personalized Cancer Care, NorthShore University Health System, Evanston, Illinois.
Brian T HelfandProgram for Personalized Cancer Care, NorthShore University Health System, Evanston, Illinois.
William IsaacsDepartment of Urology, The James Buchanan Brady Urologic Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland.ORCID 0000-0001-6599-6775
Jianfeng XuProgram for Personalized Cancer Care, NorthShore University Health System, Evanston, Illinois.
Ambry Genetics (United States) · USNorthShore University HealthSystem · USJohns Hopkins University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenome-wide association studies have identified over 100 single-nucleotide polymorphisms (SNPs) associated with prostate cancer (PrCa), and polygenic risk scores (PRS) based on their combined genotypes have been developed for risk stratification. We aimed to assess the contribution of PRS to PrCa risk in a large multisite study.

methodsThe sample included 1972 PrCa cases and 1919 unaffected controls. Next-generation sequencing was used to assess pathogenic variants in 14 PrCa-susceptibility genes and 72 validated PrCa-associated SNPs. We constructed a population-standardized PRS and tested its association with PrCa using logistic regression adjusted for age and family history of PrCa.

resultsThe mean age of PrCa cases at diagnosis and age of controls at testing/last clinic visit was 59.5 ± 7.2 and 57.2 ± 13.0 years, respectively. Among 1740 cases with pathology data, 57.4% had Gleason score ≤ 6, while 42.6% had Gleason score ≥ 8. In addition, 39.6% cases and 20.1% controls had a family history of PrCa. The PRS was significantly higher in cases than controls (mean ± SD: 1.42 ± 1.11 vs 1.02 ± 0.76; P < .0001). Compared with men in the 1st quartile of age-adjusted PRS, those in the 2nd, 3rd, and 4th quartile were 1.58 (95% confidence interval [CI]: 1.31-1.90), 2.36 (95% CI: 1.96-2.84), and 3.98 (95% CI: 3.29-4.82) times as likely to have PrCa (all P < .0001). Adjustment for family history yielded similar results. PRS predictive performance was consistent with prior literature (area under the receiver operating curve = 0.64; 95% CI: 0.62-0.66).

conclusionsThese data suggest that a 72-SNP PRS is predictive of PrCa, supporting its potential use in clinical risk assessment.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdultAgedCase-Control StudiesGenome-Wide Association StudyGenotypeHigh-Throughput Nucleotide SequencingHumansMaleMiddle AgedNeoplasm GradingProstatic NeoplasmsRisk Assessmentpolygenicprostate cancer

Identifiers

PMID33258481
PMCPMC7590110
OpenAlexW3082138385

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.