Evidence map›Paper›PMID 26010308›Full record

ArticleThe American journal of gastroenterology2015

The Presence of Genetic Mutations at Key Loci Predicts Progression to Esophageal Adenocarcinoma in Barrett's Esophagus.

Swathi Eluri, William R Brugge, Ebubekir S Daglilar, Sara A Jackson, Mindi A Styn, Keith M Callenberg, Derek C Welch, Todd M Barr, Lucas C Duits, Jacques J Bergman and 1 more

Open access · greenAbstract read
In one paragraph

Article in The American journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Emerging Biomarkers for Managing Barrett's Esophagus.Gastrointestinal endoscopy clinics of North America · 2026
    Review
  3. Article
  4. Review
  5. Molecular biomarkers of progression from Barrett's esophagus to esophageal adenocarcinoma.Frontiers in gastroenterology (Lausanne, Switzerland) · 2023
    Article
  6. Utility of ancillary studies in the diagnosis and risk assessment of Barrett's esophagus and dysplasia.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022
    Review
  7. Article
  8. Review
  9. Differential MicroRNA Signatures in the Pathogenesis of Barrett's Esophagus.Clinical and translational gastroenterology · 2020
    Article
  10. Review
  11. Article
  12. Validation of a biomarker panel in Barrett's esophagus to predict progression to esophageal adenocarcinoma.Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus · 2018
    Article
  13. Review
  14. Article
  15. Beyond Dysplasia Grade: The Role of Biomarkers in Stratifying Risk.Gastrointestinal endoscopy clinics of North America · 2017
    Review
  16. Overview of esophageal cancer.Annals of cardiothoracic surgery · 2017
    Article
  17. A Tissue Systems Pathology Test Detects Abnormalities Associated with Prevalent High-Grade Dysplasia and Esophageal Cancer in Barrett's Esophagus.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2017
    Article
  18. Review
  19. A Tissue Systems Pathology Assay for High-Risk Barrett's Esophagus.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2016
    Article
  20. Article
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

11 authors at 4 institutions in 2 countries.

Swathi EluriDivision of Gastroenterology and Hepatology, University of North Carolina, Chapel Hill, North Carolina, USA.
William R BruggeGastrointestinal Unit, Massachusetts General Hospital, Boston, Massachusetts, USA.
Ebubekir S DaglilarGastrointestinal Unit, Massachusetts General Hospital, Boston, Massachusetts, USA.
Sara A JacksonInterpace Diagnostics Corporation, Pittsburgh, Pennsylvania, USA.
Mindi A StynInterpace Diagnostics Corporation, Pittsburgh, Pennsylvania, USA.
Keith M CallenbergInterpace Diagnostics Corporation, Pittsburgh, Pennsylvania, USA.
Derek C WelchPathgroup, Brentwood, Tennessee, USA.
Todd M BarrDepartment of Pathology and Laboratory Medicine, Allegheny General Hospital, Pittsburgh, Pennsylvania, USA.
Lucas C DuitsDepartment of Gastroenterology and Hepatology, Academic Medical Center, Amsterdam, The Netherlands.
Jacques J BergmanDepartment of Gastroenterology and Hepatology, Academic Medical Center, Amsterdam, The Netherlands.
Nicholas J ShaheenDivision of Gastroenterology and Hepatology, University of North Carolina, Chapel Hill, North Carolina, USA.
Dentsply Sirona (United States) · USUniversity of North Carolina at Chapel Hill · USMassachusetts General Hospital · USMedpace (United States) · US

Funding

DIGESTIVE DISEASES EPIDEMIOLOGY TRAINING PROGRAMT32DK007634 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ROBERT S. SANDLER · 1990 to 2026
$7.4M
Non-Endoscopic Surveillance for Barrett's Esophagus Following Ablative TherapyK24DK100548 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SHAHEEN, NICHOLAS J · 2013 to 2017
$896k
NIDDK NIH HHS K24 DK100548NIDDK NIH HHS T32 DK007634
6 · The paper itself

Abstract

objectivesRisk stratification in Barrett's esophagus (BE) is challenging. We evaluated the ability of a panel of genetic markers to predict progression to high-grade dysplasia (HGD) or esophageal adenocarcinoma (EAC).

methodsIn this case-control study, we assessed a measure of genetic instability, the mutational load (ML), in predicting progression to HGD or EAC. Cases had nondysplastic BE or low-grade dysplasia (LGD) at baseline and developed HGD/EAC ≥1 year later. Controls were matched 2:1, had nondysplastic BE or LGD, and no progression at follow-up. Formalin-fixed, paraffin-embedded tissue was microdissected for the epithelium. Loss of heterozygosity (LOH) and microsatellite instability (MSI) were assessed. ML was calculated from derangements in 10 genomic loci. High-clonality LOH mutations were assigned a value of 1, low-clonality mutations were assigned a value of 0.5, and MSI 0.75 at the first loci, and 0.5 for additional loci. These values were summed to the ML. Receiver operator characteristic (ROC) curves were created.

resultsThere were 69 patients (46 controls and 23 cases). Groups were similar in age, follow-up time, baseline histology, and the number of microdissected targets. Mean ML in pre-progression biopsies was higher in cases (2.21) than in controls (0.42; P<0.0001). Sensitivity was 100% at ML ≥0.5 and specificity was 96% at ML ≥1.5. Accuracy was highest at 89.9% for ML ≥1. ROC curves for ML ≥1 demonstrated an area under the curve (AUC) of 0.95.

conclusionsML in pre-progression BE tissue predicts progression to HGD or EAC. Although further validation is necessary, ML may have utility as a biomarker in endoscopic surveillance of BE.

Indexed as

Microsatellite InstabilityAdenocarcinomaBarrett EsophagusCase-Control StudiesDisease ProgressionEsophageal NeoplasmsFemaleGenetic Predisposition to DiseaseHumansLoss of HeterozygosityMaleMiddle AgedMutationROC Curve

Identifiers

PMID26010308
PMCPMC4471888
OpenAlexW1567900071

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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 OpenQuestion graph.