Evidence map›Paper›PMID 34687971›Full record

ArticleClinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association2022

Metabolic Syndrome and Risk of Gastrointestinal Cancers: An Investigation Using Large-scale Molecular Data.

Joseph A Rothwell, Mazda Jenab, Mojgan Karimi, Thérèse Truong, Yahya Mahamat-Saleh, Pietro Ferrari, S Ghazaleh Dashti, Tilman Kühn, Amanda J Cross, Gianluca Severi and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 4 pooled it
1.6field-weighted citation impact, top 16% 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

25 citing papers in PubMed, 4 syntheses or guidelines pooled it, 32 citations in OpenAlex.

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  17. Do Polygenic Risk Scores Add to Clinical Data in Predicting Pancreatic Cancer? A Scoping Review.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2023
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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

12 authors at 5 institutions in 5 countries.

Joseph A RothwellCentre for Epidemiology and Population Health (U1018), Exposome and Heredity Team, Faculté de Médecine, Université Paris-Saclay, UVSQ, INSERM, Gustave Roussy, F-94805, Villejuif, France. Electronic address: joseph.rothwell@inserm.fr.
Mazda JenabNutrition and Metabolism Branch, International Agency for Research on Cancer (IARC), Lyon, France.
Mojgan KarimiCentre for Epidemiology and Population Health (U1018), Exposome and Heredity Team, Faculté de Médecine, Université Paris-Saclay, UVSQ, INSERM, Gustave Roussy, F-94805, Villejuif, France.
Thérèse TruongCentre for Epidemiology and Population Health (U1018), Exposome and Heredity Team, Faculté de Médecine, Université Paris-Saclay, UVSQ, INSERM, Gustave Roussy, F-94805, Villejuif, France.
Yahya Mahamat-SalehCentre for Epidemiology and Population Health (U1018), Exposome and Heredity Team, Faculté de Médecine, Université Paris-Saclay, UVSQ, INSERM, Gustave Roussy, F-94805, Villejuif, France.
Pietro FerrariNutrition and Metabolism Branch, International Agency for Research on Cancer (IARC), Lyon, France.
S Ghazaleh DashtiClinical Epidemiology and Biostatistics Unit, Murdoch Children's Research Institute, Royal Children's Hospital, Victoria, Australia.
Tilman KühnInstitute for Global Food Security (IGFS), Queen's University Belfast, United Kingdom; Heidelberg Institute of Global Health (HIGH), University of Heidelberg, Heidelberg, Germany.
Amanda J CrossDepartment of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom.
Gianluca SeveriCentre for Epidemiology and Population Health (U1018), Exposome and Heredity Team, Faculté de Médecine, Université Paris-Saclay, UVSQ, INSERM, Gustave Roussy, F-94805, Villejuif, France; Department of Statistics, Computer Science, Applications "G. Parenti," University of Florence, Italy.
Marc J GunterNutrition and Metabolism Branch, International Agency for Research on Cancer (IARC), Lyon, France.
Neil MurphyNutrition and Metabolism Branch, International Agency for Research on Cancer (IARC), Lyon, France.
Inserm · FRCentre international de recherche sur le cancer · FRImperial College London · GBQueen's University Belfast · GBRoyal Children's Hospital · AU

Funding

Medical Research Council MC_PC_17228Medical Research Council MC_QA137853World Health Organization 001
6 · The paper itself

Abstract

BACKGROUND &

aimsGastrointestinal cancer risk is influenced by the presence of metabolic syndrome (MetS). However, previous epidemiologic studies lacked full serological biomarker data for the classification of MetS, and the interaction of MetS with germline cancer risk variants is unknown.

methodsWe investigated the associations between MetS and gastrointestinal cancer risk (overall, colorectal, pancreatic, esophageal adenocarcinoma, esophageal squamous cell carcinoma, stomach cardia, stomach non-cardia, hepatocellular carcinoma, and intrahepatic bile duct cancer) in 366,016 United Kingdom Biobank participants with comprehensive serum biomarker and genotype data. MetS status was determined by 3 different definitions at baseline, and, in 15,152 participants, at a repeat assessment after a median of 4.3 years of follow-up. Multivariable hazard ratios and 95% confidence intervals for cancer outcomes were estimated using Cox proportional hazards models. Analyses stratified by polygenic risk score were conducted for colorectal and pancreatic cancers.

resultsDuring a median follow-up of 7.1 years, 4238 incident cases of a gastrointestinal cancer occurred. MetS at baseline was associated with higher risk of overall gastrointestinal cancer by any definition (hazard ratio, 1.21; 95% confidence interval, 1.13-1.29, harmonized definition). MetS was associated with increased risks of colorectal cancer, colon cancer, rectal cancer, hepatocellular carcinoma, pancreatic cancer in women, and esophageal adenocarcinoma in men. Associations for colorectal cancer and pancreatic cancer did not differ by polygenic risk score strata (P-heterogeneity 0.70 and 0.69, respectively), and 80% of participants with MetS at baseline retained this status at the repeat assessment.

conclusionsThese findings underscore the importance of maintaining good metabolic health in reducing the burden of gastrointestinal cancers, irrespective of genetic predisposition.

Indexed as

AdenocarcinomaCarcinoma, HepatocellularEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaLiver NeoplasmsMetabolic SyndromePancreatic NeoplasmsRectal NeoplasmsFemaleHumansMaleProspective StudiesRisk FactorsCancer Genetic RiskCancer PreventionGastrointestinal NeoplasmsMolecular Epidemiology

Identifiers

PMID34687971
PMCPMC9117007
OpenAlexW3207382076

What Socratic 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 Socratic graph.