Evidence map›Paper›PMID 35085228›Full record

ArticlePLoS medicine2022

The relationship between lipoprotein A and other lipids with prostate cancer risk: A multivariable Mendelian randomisation study.

Anna Ioannidou, Eleanor L Watts, Aurora Perez-Cornago, Elizabeth A Platz, Ian G Mills, Timothy J Key, Ruth C Travis, PRACTICAL consortium, CRUK, BPC3, CAPS, PEGASUS, Konstantinos K Tsilidis, Verena Zuber

Open access · goldAbstract read
In one paragraph

Article in PLoS medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 4 pooled it
4.7field-weighted citation impact, top 3% 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

33 citing papers in PubMed, 4 syntheses or guidelines pooled it, 50 citations in OpenAlex.

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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

10 authors at 5 institutions in 4 countries.

Anna IoannidouDepartment of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom.ORCID 0000-0003-2795-8174
Eleanor L WattsCancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom.ORCID 0000-0001-9229-2589
Aurora Perez-CornagoCancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom.ORCID 0000-0002-5652-356X
Elizabeth A PlatzDepartment of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America.ORCID 0000-0003-3676-8954
Ian G MillsNuffield Department of Surgical Sciences, University of Oxford, Oxford, United Kingdom.
Timothy J KeyCancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom.ORCID 0000-0003-2294-307X
Ruth C TravisCancer Epidemiology Unit, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom.ORCID 0000-0002-9571-0763
PRACTICAL consortium, CRUK, BPC3, CAPS, PEGASUS
Konstantinos K TsilidisDepartment of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom.ORCID 0000-0002-8452-8472
Verena ZuberDepartment of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom.ORCID 0000-0001-9827-1877
University of Oxford · GBImperial College London · GBJohns Hopkins University · USQueen's University Belfast · GBUniversity of Ioannina · GR

Funding

SWOG NCORP Research BaseUG1CA189974 · NCI · THE HOPE FOUNDATION · PI CHARLES D. BLANKE, DAWN HERSHMAN · 2014 to 2026
$80.6M
PCPT and SELECT Cohorts: Core Infrastructure Support for Cancer ResearchU01CA182883 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI TANGEN, CATHERINE M., THOMPSON, IAN M. · 2019 to 2023
$5.4M
PCPT and SELECT cohorts: Core Infrastructure Support for Cancer Research UM1CA182883 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI TANGEN, CATHERINE M., THOMPSON, IAN M. · 2013 to 2017
$5.2M
Cancer Research UK 28516Cancer Research UK 29017Cancer Research UK 29019Cancer Research UK C18281/A29019Cancer Research UK C60192/A28516Medical Research Council MR/W029790/1NCI NIH HHS U01 CA182883NCI NIH HHS UG1 CA189974NCI NIH HHS UM1 CA182883
6 · The paper itself

Abstract

backgroundNumerous epidemiological studies have investigated the role of blood lipids in prostate cancer (PCa) risk, though findings remain inconclusive to date. The ongoing research has mainly involved observational studies, which are often prone to confounding. This study aimed to identify the relationship between genetically predicted blood lipid concentrations and PCa. METHODS AND

findingsData for low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, triglycerides (TG), apolipoprotein A (apoA) and B (apoB), lipoprotein A (Lp(a)), and PCa were acquired from genome-wide association studies in UK Biobank and the PRACTICAL consortium, respectively. We used a two-sample summary-level Mendelian randomisation (MR) approach with both univariable and multivariable (MVMR) models and utilised a variety of robust methods and sensitivity analyses to assess the possibility of MR assumptions violation. No association was observed between genetically predicted concentrations of HDL, TG, apoA and apoB, and PCa risk. Genetically predicted LDL concentration was positively associated with total PCa in the univariable analysis, but adjustment for HDL, TG, and Lp(a) led to a null association. Genetically predicted concentration of Lp(a) was associated with higher total PCa risk in the univariable (ORweighted median per standard deviation (SD) = 1.091; 95% CI 1.028 to 1.157; P = 0.004) and MVMR analyses after adjustment for the other lipid traits (ORIVW per SD = 1.068; 95% CI 1.005 to 1.134; P = 0.034). Genetically predicted Lp(a) was also associated with advanced (MVMR ORIVW per SD = 1.078; 95% CI 0.999 to 1.163; P = 0.055) and early age onset PCa (MVMR ORIVW per SD = 1.150; 95% CI 1.015,1.303; P = 0.028). Although multiple estimation methods were utilised to minimise the effect of pleiotropy, the presence of any unmeasured pleiotropy cannot be excluded and may limit our findings.

conclusionsWe observed that genetically predicted Lp(a) concentrations were associated with an increased PCa risk. Future studies are required to understand the underlying biological pathways of this finding, as it may inform PCa prevention through Lp(a)-lowering strategies.

Indexed as

Genome-Wide Association StudyApolipoproteinsCholesterol, HDLCholesterol, LDLHumansLipidsLipoprotein(a)MaleMendelian Randomization AnalysisProstatic NeoplasmsUnited KingdomApolipoproteinsCholesterol, HDLCholesterol, LDLLipidsLipoprotein(a)

Identifiers

PMID35085228
PMCPMC8794090
OpenAlexW4225363012

What OpenQuestion holds

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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.