Evidence map›Paper›PMID 34973296›Full record

ArticleGastroenterology2022

Clonal Transitions and Phenotypic Evolution in Barrett's Esophagus.

James A Evans, Emanuela Carlotti, Meng-Lay Lin, Richard J Hackett, Magnus J Haughey, Adam M Passman, Lorna Dunn, George Elia, Ross J Porter, Mairi H McLean and 11 more

Open access · hybridAbstract read
In one paragraph

Article in Gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Mechanisms and pathophysiology of Barrett oesophagus.Nature reviews. Gastroenterology & hepatology · 2022
    Review
  20. Cell plasticity in regeneration in the stomach and beyond.Current opinion in genetics & development · 2022
    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

21 authors at 7 institutions in 1 country.

James A EvansClonal Dynamics in Epithelia Laboratory, Queen Mary University of London, London, United Kingdom.
Emanuela CarlottiClonal Dynamics in Epithelia Laboratory, Queen Mary University of London, London, United Kingdom.
Meng-Lay LinClonal Dynamics in Epithelia Laboratory, Queen Mary University of London, London, United Kingdom.
Richard J HackettClonal Dynamics in Epithelia Laboratory, Queen Mary University of London, London, United Kingdom.
Magnus J HaugheySchool of Mathematical Sciences, Queen Mary University of London, London, United Kingdom.
Adam M PassmanClonal Dynamics in Epithelia Laboratory, Queen Mary University of London, London, United Kingdom.
Lorna DunnNorthern Institute for Cancer Research, Newcastle University, Newcastle, United Kingdom.
George EliaClonal Dynamics in Epithelia Laboratory, Queen Mary University of London, London, United Kingdom.
Ross J PorterDepartment of Gastroenterology, University of Aberdeen, Aberdeen, United Kingdom.
Mairi H McLeanDepartment of Gastroenterology, University of Aberdeen, Aberdeen, United Kingdom.
Frances HughesDepartment of Surgery, Barts Health NHS Trust, Royal London Hospital, London, United Kingdom.
Joanne ChinAleongDepartment of Histopathology, Barts Health NHS Trust, Royal London Hospital, London, United Kingdom.
Philip WoodlandEndoscopy Unit, Barts Health NHS Trust, Royal London Hospital, London, United Kingdom.
Sean L PrestonEndoscopy Unit, Barts Health NHS Trust, Royal London Hospital, London, United Kingdom.
S Michael GriffinSchool of Mathematical Sciences, Queen Mary University of London, London, United Kingdom; Royal College of Surgeons of Edinburgh, Edinburgh, United Kingdom.
Laurence LovatOeosophagogastric Disorders Centre, Department of Gastroenterology, University College London Hospitals, London, United Kingdom; Research Department of Tissue and Energy, University College London Division of Surgical and Interventional Science, University College London, London, United Kingdom.
Manuel Rodriguez-JustoDepartment of Cellular Pathology, University College London Hospitals, London, United Kingdom.
Weini HuangSchool of Mathematical Sciences, Queen Mary University of London, London, United Kingdom.
Nicholas A WrightEpithelial Stem Cell Laboratory, Centre for Cancer Genomics and Computational Biology, Barts Cancer Institute, Queen Mary University of London, London, United Kingdom.
Marnix JansenDepartment of Cellular Pathology, University College London Hospitals, London, United Kingdom; UCL Cancer Institute, University College London, London, United Kingdom.
Stuart A C McDonaldClonal Dynamics in Epithelia Laboratory, Queen Mary University of London, London, United Kingdom. Electronic address: s.a.mcdonald@qmul.ac.uk.
Queen Mary University of London · GBBarts Health NHS Trust · GBRoyal London Hospital · GBUniversity of Aberdeen · GBNewcastle University · GBRoyal College of Surgeons of Edinburgh · GBUniversity College Hospital · GB

Funding

Cancer Research UK 21446Cancer Research UK A12446Cancer Research UK C16420/A18066
6 · The paper itself

Abstract

BACKGROUND &

aimsBarrett's esophagus (BE) is a risk factor for esophageal adenocarcinoma but our understanding of how it evolves is poorly understood. We investigated BE gland phenotype distribution, the clonal nature of phenotypic change, and how phenotypic diversity plays a role in progression.

methodsUsing immunohistochemistry and histology, we analyzed the distribution and the diversity of gland phenotype between and within biopsy specimens from patients with nondysplastic BE and those who had progressed to dysplasia or had developed postesophagectomy BE. Clonal relationships were determined by the presence of shared mutations between distinct gland types using laser capture microdissection sequencing of the mitochondrial genome.

resultsWe identified 5 different gland phenotypes in a cohort of 51 nondysplastic patients where biopsy specimens were taken at the same anatomic site (1.0-2.0 cm superior to the gastroesophageal junction. Here, we observed the same number of glands with 1 and 2 phenotypes, but 3 phenotypes were rare. We showed a common ancestor between parietal cell-containing, mature gastric (oxyntocardiac) and goblet cell-containing, intestinal (specialized) gland phenotypes. Similarly, we have shown a clonal relationship between cardiac-type glands and specialized and mature intestinal glands. Using the Shannon diversity index as a marker of gland diversity, we observed significantly increased phenotypic diversity in patients with BE adjacent to dysplasia and predysplasia compared to nondysplastic BE and postesophagectomy BE, suggesting that diversity develops over time.

conclusionsWe showed that the range of BE phenotypes represents an evolutionary process and that changes in gland diversity may play a role in progression. Furthermore, we showed a common ancestry between gastric and intestinal-type glands in BE.

Indexed as

Barrett EsophagusEsophageal NeoplasmsEsophagogastric JunctionHumansPhenotypeBarrett’s Esophagus (BE)ClonalDiversityEsophageal Adenocarcinoma (EA)Evolution

Identifiers

PMID34973296
PMCPMC8972067
OpenAlexW4210691555

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.