Evidence map›Paper›PMID 38958976›Full record

ArticleJAMA network open2024

Early Prostate Cancer Deaths Among Men With Higher vs Lower Genetic Risk.

Anna Plym, Yiwen Zhang, Konrad H Stopsack, Emilio Ugalde-Morales, Tyler M Seibert, David V Conti, Christopher A Haiman, Aris Baras, Tanja Stocks, Isabel Drake and 6 more

Abstract read
In one paragraph

Article in JAMA network open, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–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

10 citing papers in PubMed.

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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

16 authors.

Anna PlymDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Yiwen ZhangDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts.
Konrad H StopsackDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts.
Emilio Ugalde-MoralesDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Tyler M SeibertDepartment of Radiation Medicine and Applied Sciences, Department of Radiology, and Department of Bioengineering, University of California San Diego, La Jolla.
David V ContiCenter for Genetic Epidemiology, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles.
Christopher A HaimanCenter for Genetic Epidemiology, Department of Population and Public Health Sciences, Keck School of Medicine, University of Southern California, Los Angeles.
Aris BarasRegeneron Genetics Center, Tarrytown, New York.
Tanja StocksDepartment of Translational Medicine, Lund University, Malmö, Sweden.
Isabel DrakeDepartment of Clinical Sciences in Malmö, Lund University, Malmö, Sweden.
Kathryn L PenneyDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts.
Edward GiovannucciDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts.
Adam S KibelDepartment of Urology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Fredrik WiklundDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Lorelei A MucciDepartment of Epidemiology, Harvard T. H. Chan School of Public Health, Boston, Massachusetts.
Regeneron Genetics Center

Funding

Cancer Epidemiology Cohort in Male Health ProfessionalsU01CA167552 · NCI · HARVARD UNIVERSITY D/B/A HARVARD SCHOOL OF PUBLIC HEALTH · PI Lorelei Mucci, Walter C. Willett · 2017 to 2026
$17.0M
The Impact of DNA Damage Repair Abnormalities in Prostate CancerP01CA228696 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI OFFIT, KENNETH, POMERANTZ, MARK M. · 2019 to 2024
$8.7M
Leveraging Prospective Cancer Epidemiology Cohorts and Novel Methods to Improve Polygenic Risk ScoresU01CA261339 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Fei Chen, David V Conti · 2021 to 2026
$5.2M
NCI NIH HHS P01 CA228696NCI NIH HHS U01 CA167552NCI NIH HHS U01 CA261339
6 · The paper itself

Abstract

Importance: Prostate cancer, a leading cause of cancer death among men, urgently requires new prevention strategies, which may involve targeting men with an underlying genetic susceptibility. Objective: To explore differences in risk of early prostate cancer death among men with higher vs lower genetic risk to inform prevention efforts. Design, Setting, and Participants: This cohort study used a combined analysis of genotyped men without prostate cancer at inclusion and with lifestyle data in 2 prospective cohort studies in Sweden and the US, the Malmö Diet and Cancer Study (MDCS) and the Health Professionals Follow-Up Study (HPFS), followed up from 1991 to 2019. Data were analyzed between April 2023 and April 2024. Exposures: Men were categorized according to modifiable lifestyle behaviors and genetic risk. A polygenic risk score above the median or a family history of cancer defined men at higher genetic risk (67% of the study population); the remaining men were categorized as being at lower genetic risk. Main Outcomes and Measures: Prostate cancer death analyzed using time-to-event analysis estimating hazard ratios (HR), absolute risks, and preventable deaths by age. Results: Among the 19 607 men included for analysis, the median (IQR) age at inclusion was 59.0 (53.0-64.7) years (MDCS) and 65.1 (58.0-71.8) years (HPFS). During follow-up, 107 early (by age 75 years) and 337 late (after age 75 years) prostate cancer deaths were observed. Compared with men at lower genetic risk, men at higher genetic risk had increased rates of both early (HR, 3.26; 95% CI, 1.82-5.84) and late (HR, 2.26; 95% CI, 1.70-3.01) prostate cancer death, and higher lifetime risks of prostate cancer death (3.1% vs 1.3% [MDCS] and 2.3% vs 0.6% [HPFS]). Men at higher genetic risk accounted for 94 of 107 early prostate cancer deaths (88%), of which 36% (95% CI, 12%-60%) were estimated to be preventable through adherence to behaviors associated with a healthy lifestyle (not smoking, healthy weight, high physical activity, and a healthy diet). Conclusions and Relevance: In this 20-year follow-up study, men with a genetic predisposition accounted for the vast majority of early prostate cancer deaths, of which one-third were estimated to be preventable. This suggests that men at increased genetic risk should be targeted in prostate cancer prevention strategies.

Indexed as

Genetic Predisposition to DiseaseProstatic NeoplasmsAgedCohort StudiesHumansLife StyleMaleMiddle AgedProspective StudiesRisk FactorsSwedenUnited States

Identifiers

PMID38958976
PMCPMC11222990

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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.