Evidence map›Paper›PMID 36320039›Full record

ArticleBMC medicine2022

Mendelian randomization analysis of factors related to ovulation and reproductive function and endometrial cancer risk.

Shannon D'Urso, Pooja Arumugam, Therese Weider, Liang-Dar Hwang, Tom A Bond, John P Kemp, Nicole M Warrington, David M Evans, Tracy A O'Mara, Gunn-Helen Moen

Open access · goldAbstract read
In one paragraph

Article in BMC medicine, 2022. 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
1.8field-weighted citation impact, top 13% 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

10 citing papers in PubMed, 20 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 3 institutions in 3 countries.

Shannon D'UrsoInstitute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
Pooja ArumugamSchool of Biomedical Sciences, Faculty of Medicine, The University of Queensland, Brisbane, Australia.
Therese WeiderInstitute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Liang-Dar HwangInstitute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
Tom A BondMRC Integrative Epidemiology Unit at the University of Bristol, Bristol, UK.
John P KempInstitute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
Nicole M WarringtonInstitute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
David M EvansInstitute for Molecular Bioscience, The University of Queensland, Brisbane, Australia.
Tracy A O'MaraCancer Research Program, QIMR Berghofer Medical Research Institute, Brisbane, QLD, Australia.
Gunn-Helen MoenInstitute for Molecular Bioscience, The University of Queensland, Brisbane, Australia. g.h.moen@medisin.uio.no.ORCID 0000-0002-8768-0904
The University of Queensland · AUOslo University Hospital · NOQIMR Berghofer Medical Research Institute · AU

Funding

Medical Research Council MC_PC_17228Medical Research Council MC_QA137853Medical Research Council MC_UU_00011/6
6 · The paper itself

Abstract

backgroundObservational epidemiological studies suggest a link between several factors related to ovulation and reproductive function and endometrial cancer (EC) risk; however, it is not clear whether these relationships are causal, and whether the risk factors act independently of each other. The aim of this study was to investigate putative causal relationships between the number of live births, age at last live birth, and years ovulating and EC risk. 

methodsWe conducted a series of observational analyses to investigate various risk factors and EC risk in the UK Biobank (UKBB). Additionally, multivariate analysis was performed to elucidate the relationship between the number of live births, age at last live birth, and years ovulating and other related factors such as age at natural menopause, age at menarche, and body mass index (BMI). Secondly, we used Mendelian randomization (MR) to assess if these observed relationships were causal. Genome-wide significant single nucleotide polymorphisms (SNPs) were extracted from previous studies of woman's number of live births, age at menopause and menarche, and BMI. We conducted a genome-wide association analysis using the UKBB to identify SNPs associated with years ovulating, years using the contraceptive pill, and age at last live birth.

resultsWe found evidence for a causal effect of the number of live births (inverse variance weighted (IVW) odds ratio (OR): 0.537, p = 0.006), the number of years ovulating (IVW OR: 1.051, p = 0.014), in addition to the known risk factors BMI, age at menarche, and age at menopause on EC risk in the univariate MR analyses. Due to the close relationships between these factors, we followed up with multivariable MR (MVMR) analysis. Results from the MVMR analysis showed that number of live births had a causal effect on EC risk (OR: 0.783, p = 0.036) independent of BMI, age at menarche and age at menopause.

conclusionsMVMR analysis showed that the number of live births causally reduced the risk of EC.

Indexed as

Endometrial NeoplasmsMendelian Randomization AnalysisBody Mass IndexFemaleGenome-Wide Association StudyHumansOvulationPolymorphism, Single NucleotideRisk FactorsAge at last live birthEndometrial cancerFertilityGWASMendelian randomizationNumber of live birthsUK biobankYears ovulating

Identifiers

PMID36320039
PMCPMC9623961
OpenAlexW4308019623

What OpenQuestion holds

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LicenceCC BY
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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.