Evidence map›Paper›PMID 37599317›Full record

SynthesisJournal of cancer research and clinical oncology2023

Genetically determined circulating resistin concentrations and risk of colorectal cancer: a two-sample Mendelian randomization study.

Thu Thi Pham, Katharina Nimptsch, Nikos Papadimitriou, Krasimira Aleksandrova, Mazda Jenab, Marc J Gunter, Loic Le Marchand, Li Li, Brigid M Lynch, Sergi Castellví-Bel and 6 more

Open access · hybridAbstract readMeta-Analysis
In one paragraph

Synthesis in Journal of cancer research and clinical oncology, 2023. 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
0.6field-weighted citation impact, top 28% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  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

16 authors at 14 institutions in 6 countries.

Thu Thi PhamMolecular Epidemiology Research Group, Max Delbrueck Center for Molecular Medicine in the Helmholtz Association (MDC), 13125, Berlin, Germany.
Katharina NimptschMolecular Epidemiology Research Group, Max Delbrueck Center for Molecular Medicine in the Helmholtz Association (MDC), 13125, Berlin, Germany.
Nikos PapadimitriouNutrition and Metabolism Branch, International Agency for Research on Cancer (IARC-WHO), World Health Organization, 150 Cours Albert Thomas, 69372, Lyon, Cedex 08, France.
Krasimira AleksandrovaDepartment of Epidemiological Methods and Etiological Research, Leibniz Institute for Prevention Research and Epidemiology-BIPS, 28359, Bremen, Germany.
Mazda JenabNutrition and Metabolism Branch, International Agency for Research on Cancer (IARC-WHO), World Health Organization, 150 Cours Albert Thomas, 69372, Lyon, Cedex 08, France.
Marc J GunterNutrition and Metabolism Branch, International Agency for Research on Cancer (IARC-WHO), World Health Organization, 150 Cours Albert Thomas, 69372, Lyon, Cedex 08, France.
Loic Le MarchandEpidemiology Program, University of Hawaii Cancer Center, Honolulu, HI, 96813, USA.
Li LiDepartment of Family Medicine and UVA Comprehensive Cancer Center, University of Virginia, Charlottesville, Virginia, USA.
Brigid M LynchCancer Epidemiology Division, Cancer Council Victoria, Melbourne, Australia.
Sergi Castellví-BelDepartment of Gastroenterology, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Hospital Clínic, Universitat de Barcelona, Barcelona, Spain.
Amanda I PhippsFred Hutchinson Cancer Center, Seattle, WA, USA.
Stephanie L SchmitGenomic Medicine Institute, Cleveland Clinic, Cleveland, OH, USA.
Hermann BrennerDivision of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Shuji OginoProgram in Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Edward GiovannucciDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Tobias PischonMolecular Epidemiology Research Group, Max Delbrueck Center for Molecular Medicine in the Helmholtz Association (MDC), 13125, Berlin, Germany. tobias.pischon@mdc-berlin.de.
Centre international de recherche sur le cancer · FRBerlin Institute of Health at Charité - Universitätsmedizin Berlin · DECancer Council Victoria · AUCleveland Clinic · USDana-Farber/Harvard Cancer Center · USFreie Universität Berlin · DEHarvard University · USMax Delbrück Center · DENational Center for Tumor Diseases · DESeattle University · USUniversitat de Barcelona · ESUniversity of Bremen · DEUniversity of Hawaiʻi at Mānoa · USUniversity of Virginia · US

Funding

Data sharing: the Colon Cancer Family Registry CohortU01CA167551 · NCI · UNIVERSITY OF MELBOURNE · PI Daniel David BUCHANAN, Steven Gallinger · 2018 to 2026
$16.8M
NCI NIH HHS U01 CA167551World Health Organization 001
6 · The paper itself

Abstract

purposeResistin, a novel pro-inflammatory protein implicated in inflammatory processes, has been suggested to play a role in colorectal development. However, evidence from observational studies has been inconsistent. Mendelian randomization may be a complementary method to examine this association.

methodsWe conducted a two-sample Mendelian randomization to estimate the association between genetically determined circulating resistin concentrations and risk of colorectal cancer (CRC). Protein quantitative trait loci (pQTLs) from the SCALLOP consortium were used as instrumental variables (IVs) for resistin. CRC genetic summary data was obtained from GECCO/CORECT/CCFR (the Genetics and Epidemiology of Colorectal Cancer Consortium, Colorectal Cancer Transdisciplinary Study, and Colon Cancer Family Registry), and FinnGen (Finland Biobank). The inverse variance weighted method (IVW) was applied in the main analysis, and other robust methods were used as sensitivity analyses. Estimates for the association from the two data sources were then pooled using a meta-analysis approach.

resultsThirteen pQTLs were identified as IVs explaining together 7.80% of interindividual variation in circulating resistin concentrations. Based on MR analyses, genetically determined circulating resistin concentrations were not associated with incident CRC (pooled-IVW-OR per standard deviation of resistin, 1.01; 95% CI 0.96, 1.06; p = 0.67. Restricting the analyses to using IVs within or proximal to the resistin-encoding gene (cis-IVs), or to IVs located elsewhere in the genome (trans-IVs) provided similar results. The association was not altered when stratified by sex or CRC subsites.

conclusionsWe found no evidence of a relationship between genetically determined circulating resistin concentrations and risk of CRC.

Indexed as

Colonic NeoplasmsResistinGenome-Wide Association StudyHumansMendelian Randomization AnalysisPolymorphism, Single NucleotideQuantitative Trait LociResistinColorectal cancerGeneticInstrumentalMendelian randomizationResistin

Identifiers

PMID37599317
PMCPMC10602946
OpenAlexW4386019118

What Socratic 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 Socratic graph.