Evidence map›Paper›PMID 36434155›Full record

ArticleBritish journal of cancer2023

Disentangling the aetiological pathways between body mass index and site-specific cancer risk using tissue-partitioned Mendelian randomisation.

Genevieve M Leyden, Michael P Greenwood, Valérie Gaborieau, Younghun Han, Christopher I Amos, Paul Brennan, David Murphy, George Davey Smith, Tom G Richardson

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 14 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

9 authors at 3 institutions in 3 countries.

Genevieve M LeydenMRC Integrative Epidemiology Unit, Bristol Population Health Science Institute, University of Bristol, Bristol, BS8 2BN, UK. rj18633@bristol.ac.uk.ORCID http://orcid.org/0000-0002-6024-4950
Michael P GreenwoodBristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, BS1 3NY, UK.
Valérie GaborieauGenomic Epidemiology Branch, International Agency for Research on Cancer (IARC/WHO), Lyon, France.
Younghun HanInstitute for Clinical and Translational Research, Baylor College of Medicine, Houston, TX, USA.
Christopher I AmosInstitute for Clinical and Translational Research, Baylor College of Medicine, Houston, TX, USA.ORCID http://orcid.org/0000-0002-8540-7023
Paul BrennanBristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, BS1 3NY, UK.
David MurphyBristol Medical School: Translational Health Sciences, Dorothy Hodgkin Building, University of Bristol, Bristol, BS1 3NY, UK.
George Davey SmithMRC Integrative Epidemiology Unit, Bristol Population Health Science Institute, University of Bristol, Bristol, BS8 2BN, UK.ORCID http://orcid.org/0000-0002-1407-8314
Tom G RichardsonMRC Integrative Epidemiology Unit, Bristol Population Health Science Institute, University of Bristol, Bristol, BS8 2BN, UK. tom.g.richardson@bristol.ac.uk.ORCID http://orcid.org/0000-0002-7918-2040
University of Bristol · GBBaylor College of Medicine · USCentre international de recherche sur le cancer · FR

Funding

British Heart Foundation FS/17/60/33474Medical Research Council MC_UU_00011/1Medical Research Council MC_UU_00032/1World Health Organization 001
6 · The paper itself

Abstract

backgroundBody mass index (BMI) is known to influence the risk of various site-specific cancers, however, dissecting which subcomponents of this heterogenous risk factor are predominantly responsible for driving disease effects has proven difficult to establish. We have leveraged tissue-specific gene expression to separate the effects of distinct phenotypes underlying BMI on the risk of seven site-specific cancers.

methodsSNP-exposure estimates were weighted in a multivariable Mendelian randomisation analysis by their evidence for colocalization with subcutaneous adipose- and brain-tissue-derived gene expression using a recently developed methodology.

resultsOur results provide evidence that brain-tissue-derived BMI variants are predominantly responsible for driving the genetically predicted effect of BMI on lung cancer (OR: 1.17; 95% CI: 1.01-1.36; P = 0.03). Similar findings were identified when analysing cigarettes per day as an outcome (Beta = 0.44; 95% CI: 0.26-0.61; P = 1.62 × 10

conclusionsThe study provides valuable insight into the divergent underlying pathways between BMI and the risk of site-specific cancers.

Indexed as

Endometrial NeoplasmsLung NeoplasmsBody Mass IndexFemaleGenome-Wide Association StudyHumansObesityPolymorphism, Single NucleotideRisk Factors

Identifiers

PMID36434155
PMCPMC9938133
OpenAlexW4310058929

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.