Evidence map›Paper›PMID 39419895›Full record

ArticleCancer causes & control : CCC2025

Exploring estrogen-related mechanisms in ovarian carcinogenesis: association between bone mineral density and ovarian cancer risk in a multivariable Mendelian randomization study.

Karen M Tuesley, Penelope M Webb, Melinda M Protani, Peter Donovan, Susan J Jordan, Suzanne Dixon-Suen

Abstract read
In one paragraph

Article in Cancer causes & control : CCC, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

6 authors.

Karen M TuesleySchool of Public Health, Faculty of Medicine, The University of Queensland, Brisbane, Australia. k.tuesley@uq.edu.au.ORCID http://orcid.org/0000-0002-5944-5085
Penelope M WebbSchool of Public Health, Faculty of Medicine, The University of Queensland, Brisbane, Australia.ORCID http://orcid.org/0000-0003-0733-5930
Melinda M ProtaniSchool of Public Health, Faculty of Medicine, The University of Queensland, Brisbane, Australia.ORCID http://orcid.org/0000-0001-6452-7571
Peter DonovanClinical Pharmacology Department, Royal Brisbane and Women's Hospital, Brisbane, Australia.ORCID http://orcid.org/0000-0001-7934-601X
Susan J JordanSchool of Public Health, Faculty of Medicine, The University of Queensland, Brisbane, Australia.ORCID http://orcid.org/0000-0002-4566-1414
Suzanne Dixon-Suen *Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Australia.ORCID http://orcid.org/0000-0003-3714-8386

Funding

Australian Government Research Training Program scholarshipNational Health and Medical Research Council GNT1173346
6 · The paper itself

Abstract

backgroundEstrogen may play a role in epithelial ovarian cancer (EOC) carcinogenesis, with effects varying by EOC histotype. Measuring women's long-term exposure to estrogen is difficult, but bone mineral density (BMD) may be a reasonable proxy of longer-term exposure. We examined this relationship by assessing the association between genetic predisposition for higher BMD and risk of EOC by histotype.

methodsWe used Mendelian randomization (MR) to assess associations between genetic markers for femoral neck and lumbar spine BMD and each EOC histotype. We used multivariable MR (MVMR) to adjust for probable pleiotropic traits, including body mass index, height, menarcheal age, menopausal age, smoking, alcohol intake, and vitamin D.

resultsUnivariable analyses suggested greater BMD was associated with increased risk of endometrioid EOC (per standard deviation increase; lumbar spine OR = 1.21; 95% CI 0.93,1.57, femoral neck: OR = 1.25; 0.99,1.57), but sensitivity analyses indicated that pleiotropy was likely. Adjustment using MVMR reduced the magnitude of estimates slightly (lumbar spine: OR = 1.13; 95% CI 1.00,1.28, femoral neck: OR = 1.18; 1.03,1.36). Results for lumbar spine BMD and high-grade serous EOC were also suggestive of an association (univariable MR: OR = 1.16; 95% CI 1.03,1.30; MVMR: OR = 1.06; 0.99,1.14).

conclusionOur study found associations between genetic predisposition to higher BMD, a proxy for long-term estrogen exposure, and risk of developing endometroid and high-grade serous EOC cancers. These findings add to existing evidence of the relationship between estrogen and increased risk of EOC for certain histotypes.

Indexed as

Bone DensityEstrogensOvarian NeoplasmsCarcinoma, Ovarian EpithelialFemaleGenetic Predisposition to DiseaseHumansMendelian Randomization AnalysisMiddle AgedPolymorphism, Single NucleotideRisk FactorsEstrogensBone mineral densityEpithelial ovarian cancerMendelian randomizationOestrogen

Identifiers

PMID39419895
PMCPMC11775049

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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.