Evidence map›Paper›PMID 29247777›Full record

ArticleGastroenterology2018

Determining Risk of Barrett's Esophagus and Esophageal Adenocarcinoma Based on Epidemiologic Factors and Genetic Variants.

Jing Dong, Matthew F Buas, Puya Gharahkhani, Bradley J Kendall, Lynn Onstad, Shanshan Zhao, Lesley A Anderson, Anna H Wu, Weimin Ye, Nigel C Bird and 18 more

Abstract readMulticenter Study
In one paragraph

Article in Gastroenterology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 6 pooled it
–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

48 citing papers in PubMed, 6 syntheses or guidelines pooled it.

  1. Diagnostic Risk Prediction Models for Upper Gastrointestinal Cancers: A Systematic Review.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2025
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  7. Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026
    Review
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  10. Cancer pathogenesis and therapy · 2025
    Article
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  14. Evolution of Treatment Outcomes and Prognostic Factors in Esophageal Cancer Surgery: A Retrospective Analysis of 1500 Consecutive Esophagostomies.Annals of surgery open : perspectives of surgical history, education, and clinical approaches · 2023
    Article
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  17. Sleep Behaviors, Genetic Predispositions, and Risk of Esophageal Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2023
    Article
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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

28 authors.

Jing DongDan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, Texas.
Matthew F BuasDivision of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington; Department of Cancer Prevention and Control, Roswell Park Cancer Institute, Buffalo, New York.
Puya GharahkhaniStatistical Genetics, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia.
Bradley J KendallCancer Control, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia; School of Medicine, University of Queensland, Brisbane, Queensland, Australia; Department of Gastroenterology and Hepatology, Princess Alexandra Hospital, Brisbane, Queensland, Australia.
Lynn OnstadDivision of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington.
Shanshan ZhaoBiostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina.
Lesley A AndersonCentre for Public Health, Queen's University Belfast, Belfast, Northern Ireland.
Anna H WuDepartment of Preventive Medicine, University of Southern California/Norris Comprehensive Cancer Center, Los Angeles, California.
Weimin YeDepartment of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
Nigel C BirdDepartment of Oncology, Medical School, University of Sheffield, Sheffield, United Kingdom.
Leslie BernsteinDepartment of Population Sciences, Beckman Research Institute and City of Hope Comprehensive Cancer Center, Duarte, California.
Wong-Ho ChowDepartment of Epidemiology, MD Anderson Cancer Center, Houston, Texas.
Marilie D GammonDepartment of Epidemiology, University of North Carolina, Chapel Hill, North Carolina.
Geoffrey LiuPharmacogenomic Epidemiology, Ontario Cancer Institute, Toronto, Ontario, Canada.
Carlos CaldasCancer Research UK, Cambridge Institute, Cambridge, United Kingdom.
Paul D PharoahDepartment of Oncology, University of Cambridge, Cambridge, United Kingdom; Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom.
Harvey A RischDepartment of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, Connecticut.
Prasad G IyerDivision of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota.
Brian J ReidDivision of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington.
Laura J HardieDivision of Epidemiology, Leeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, Leeds, United Kingdom.
Jesper LagergrenDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden; School of Cancer Sciences, King's College London, London, United Kingdom.
Nicholas J ShaheenDivision of Gastroenterology and Hepatology, University of North Carolina School of Medicine, Chapel Hill, North Carolina.
Douglas A CorleyDivision of Research, Kaiser Permanente Northern California, Oakland, California; San Francisco Medical Center, Kaiser Permanente Northern California, San Francisco, California.
Rebecca C FitzgeraldMedical Research Council Cancer Unit, Hutchison-Medical Research Council Research Centre, University of Cambridge, Cambridge, United Kingdom.
Stomach and Oesophageal Cancer Study (SOCS) consortium
David C WhitemanCancer Control, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia.
Thomas L VaughanDivision of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington.
Aaron P ThriftDan L Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, Texas; Section of Epidemiology and Population Sciences, Department of Medicine, Baylor College of Medicine, Houston, Texas. Electronic address: aaron.thrift@bcm.edu.

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI MARK G FRATTINI · 1985 to 2026
$116.6M
PHYLOGENIES of Barrett's Esophagus LineagesP01CA091955 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI GRADY, WILLIAM MALLORY · 2002 to 2019
$35.9M
PILOT AND FEASIBILITY STUDIESP30DK034987 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ROBERT S. SANDLER · 1985 to 2026
$30.5M
Barrett's and Esophageal Adenocarcinoma Genetic Susceptibility Study (BEAGESS)R01CA136725 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI VAUGHAN, THOMAS L, WHITEMAN, DAVID C · 2009 to 2011
$7.8M
ESTABLISHED INVESTIGATOR AWARD IN CANCER PREVENTION AND CONTROLK05CA124911 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI VAUGHAN, THOMAS L · 2007 to 2016
$1.6M
EPIDEMIOLOGY OF BARRETTS ESOPHAGUSR01CA072866 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI VAUGHAN, THOMAS L · 1997 to 2000
$543k
Cancer Research UK 10119Cancer Research UK 16561Cancer Research UK 16942NCI NIH HHS K05 CA124911NCI NIH HHS P01 CA091955NCI NIH HHS P30 CA016056NCI NIH HHS R01 CA072866NCI NIH HHS R01 CA136725NIDDK NIH HHS P30 DK034987
6 · The paper itself

Abstract

BACKGROUND &

aimsWe developed comprehensive models to determine risk of Barrett's esophagus (BE) or esophageal adenocarcinoma (EAC) based on genetic and non-genetic factors.

methodsWe used pooled data from 3288 patients with BE, 2511 patients with EAC, and 2177 individuals without either (controls) from participants in the international Barrett's and EAC consortium as well as the United Kingdom's BE gene study and stomach and esophageal cancer study. We collected data on 23 genetic variants associated with risk for BE or EAC, and constructed a polygenic risk score (PRS) for cases and controls by summing the risk allele counts for the variants weighted by their natural log-transformed effect estimates (odds ratios) extracted from genome-wide association studies. We also collected data on demographic and lifestyle factors (age, sex, smoking, body mass index, use of nonsteroidal anti-inflammatory drugs) and symptoms of gastroesophageal reflux disease (GERD). Risk models with various combinations of non-genetic factors and the PRS were compared for their accuracy in identifying patients with BE or EAC using the area under the receiver operating characteristic curve (AUC) analysis.

resultsIndividuals in the highest quartile of risk, based on genetic factors (PRS), had a 2-fold higher risk of BE (odds ratio, 2.22; 95% confidence interval, 1.89-2.60) or EAC (odds ratio, 2.46; 95% confidence interval, 2.07-2.92) than individual in the lowest quartile of risk based on PRS. Risk models developed based on only demographic or lifestyle factors or GERD symptoms identified patients with BE or EAC with AUC values ranging from 0.637 to 0.667. Combining data on demographic or lifestyle factors with data on GERD symptoms identified patients with BE with an AUC of 0.793 and patients with EAC with an AUC of 0.745. Including PRSs with these data only minimally increased the AUC values for BE (to 0.799) and EAC (to 0.754). Including the PRSs in the model developed based on non-genetic factors resulted in a net reclassification improvement for BE of 3.0% and for EAC of 5.6%.

conclusionsWe used data from 3 large databases of patients from studies of BE or EAC to develop a risk prediction model based on genetic, clinical, and demographic/lifestyle factors. We identified a PRS that increases discrimination and net reclassification of individuals with vs without BE and EAC. However, the absolute magnitude of improvement is not sufficient to justify its clinical use.

Indexed as

Decision Support TechniquesModels, GeneticPolymorphism, Single NucleotideAdenocarcinomaArea Under CurveAustraliaBarrett EsophagusCase-Control StudiesDatabases, FactualEsophageal NeoplasmsEuropeFemaleGene-Environment InteractionGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansBEACONEnvironmental ExposuresNeoplasmSNP

Identifiers

PMID29247777
PMCPMC5880715

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Registered trials

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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.