Evidence map›Paper›PMID 42032305›Full record

ArticleCommunications medicine2026

Polygenic risk score and 20-year prostate cancer-specific mortality and survival.

Anna Plym, Anqi Wang, Konrad H Stopsack, Yiwen Zhang, Aris Baras, Regeneron Genetics Center, Isabel Drake, Mark Clements, Kathryn L Penney, Edward Giovannucci and 3 more

Abstract read
In one paragraph

Article in Communications medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Anna PlymDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. anna.plym@ki.se.ORCID http://orcid.org/0000-0001-6351-4744
Anqi WangDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
Konrad H StopsackDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.ORCID http://orcid.org/0000-0002-0722-1311
Yiwen ZhangDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
Aris BarasRegeneron Genetics Center, Tarrytown, New York, USA.
Regeneron Genetics Center
Isabel DrakeDepartment of Clinical Sciences in Malmö, Lund University, Malmö, Sweden.ORCID http://orcid.org/0000-0002-6500-6310
Mark ClementsDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Kathryn L PenneyDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
Edward GiovannucciDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.ORCID http://orcid.org/0000-0002-6123-0219
Adam S KibelDepartment of Urology, Mass General Brigham, Harvard Medical School, Boston, MA, USA.
Lorelei A Mucci *Department of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
Fredrik Wiklund *Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.ORCID http://orcid.org/0000-0002-4623-0544

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPolygenic risk scores (PRSs) strongly discriminate for prostate cancer risk at the population level. The role of these genetic scores in determining prostate cancer survival is unclear, potentially due to methodological issues.

methodsWe included 19,607 men from the Malmö Diet and Cancer Study (MDCS) and the Health Professionals Follow-up Study (HPFS) and analyzed 20-year incidence and mortality (from full cohort analyses) and survival (from case-only analyses) according to a 451-variant PRS. For most of the men included, early access to prostate-specific antigen (PSA) testing was limited.

resultsIn full cohort analyses, a PRS at or above the median (vs. below the median) shows a strong association with prostate cancer incidence (hazard ratio (HR) 3.02, 95% CI 2.78-3.28) and, somewhat stronger, with prostate cancer mortality (HR 3.26, 95% CI 2.63-4.04). As expected, case-only survival analyses of prostate cancer death show a similar direction (HR 1.21, 95% CI 0.98-1.50), which becomes stronger when excluding variants linked to PSA (HR 1.25, 95% CI, 1.01-1.54), in particular in the age group 65-74 years at diagnosis (HR 1.72, 95% CI 1.21-2.45). In the other age groups, HRs are close to or below 1. This indicates that standard case-only survival estimates may not accurately reflect risk across age, consistent with age-dependent selection mechanisms, and further points to an influence from disease detection.

conclusionsOverall, these findings support that inherited genetic risk captured by the 451-variant PRS may have an influence on prostate cancer survival.

Identifiers

PMID42032305
PMCPMC13109360

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