Alterations to the Esophageal Microbiome Associated with Progression from Barrett's Esophagus to Esophageal Adenocarcinoma.


Journal

Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
ISSN: 1538-7755
Titre abrégé: Cancer Epidemiol Biomarkers Prev
Pays: United States
ID NLM: 9200608

Informations de publication

Date de publication:
10 2019
Historique:
received: 02 01 2019
revised: 17 04 2019
accepted: 10 07 2019
pubmed: 31 8 2019
medline: 25 9 2020
entrez: 31 8 2019
Statut: ppublish

Résumé

The incidence of esophageal adenocarcinoma has risen dramatically over the past half century, and the underlying reasons are incompletely understood. Broad shifts to the upper gastrointestinal microbiome may be partly responsible. The goal of this study was to describe alterations in the esophageal microbiome that occur with progression from Barrett's esophagus to esophageal adenocarcinoma. A case-control study was performed of patients with and without Barrett's esophagus who were scheduled to undergo upper endoscopy. Demographic, clinical, and dietary intake data were collected, and esophageal brushings were collected during the endoscopy. 16S rRNA gene sequencing was performed to characterize the microbiome. A total of 45 patients were enrolled and included in the analyses [16 controls; 14 Barrett's esophagus without dysplasia (NDBE); 6 low-grade dysplasia (LGD); 5 high-grade dysplasia (HGD); and 4 esophageal adenocarcinoma]. There was no difference in alpha diversity between non-Barrett's esophagus and Barrett's esophagus, but there was evidence of decreased diversity in patients with esophageal adenocarcinoma as assessed by Simpson index. There was an apparent shift in composition at the transition from LGD to HGD, and patients with HGD and esophageal adenocarcinoma had decreased Firmicutes and increased Proteobacteria. In addition, patients with HGD or esophageal adenocarcinoma had increased Shifts in the Barrett's esophagus-associated microbiome were observed in patients with HGD and esophageal adenocarcinoma, with increases in certain potentially pathogenic bacteria. The microbiome may play a role in esophageal carcinogenesis.

Sections du résumé

BACKGROUND
The incidence of esophageal adenocarcinoma has risen dramatically over the past half century, and the underlying reasons are incompletely understood. Broad shifts to the upper gastrointestinal microbiome may be partly responsible. The goal of this study was to describe alterations in the esophageal microbiome that occur with progression from Barrett's esophagus to esophageal adenocarcinoma.
METHODS
A case-control study was performed of patients with and without Barrett's esophagus who were scheduled to undergo upper endoscopy. Demographic, clinical, and dietary intake data were collected, and esophageal brushings were collected during the endoscopy. 16S rRNA gene sequencing was performed to characterize the microbiome.
RESULTS
A total of 45 patients were enrolled and included in the analyses [16 controls; 14 Barrett's esophagus without dysplasia (NDBE); 6 low-grade dysplasia (LGD); 5 high-grade dysplasia (HGD); and 4 esophageal adenocarcinoma]. There was no difference in alpha diversity between non-Barrett's esophagus and Barrett's esophagus, but there was evidence of decreased diversity in patients with esophageal adenocarcinoma as assessed by Simpson index. There was an apparent shift in composition at the transition from LGD to HGD, and patients with HGD and esophageal adenocarcinoma had decreased Firmicutes and increased Proteobacteria. In addition, patients with HGD or esophageal adenocarcinoma had increased
CONCLUSIONS
Shifts in the Barrett's esophagus-associated microbiome were observed in patients with HGD and esophageal adenocarcinoma, with increases in certain potentially pathogenic bacteria.
IMPACT
The microbiome may play a role in esophageal carcinogenesis.

Identifiants

pubmed: 31466948
pii: 1055-9965.EPI-19-0008
doi: 10.1158/1055-9965.EPI-19-0008
pmc: PMC6774849
mid: NIHMS1534988
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1687-1693

Subventions

Organisme : NIDDK NIH HHS
ID : K23 DK111847
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI116939
Pays : United States
Organisme : NCI NIH HHS
ID : U54 CA163004
Pays : United States

Informations de copyright

©2019 American Association for Cancer Research.

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Auteurs

Erik J Snider (EJ)

Department of Medicine, University of Washington School of Medicine, Seattle, Washington.

Griselda Compres (G)

Department of Medicine, Columbia University Irving Medical Center, New York, New York.

Daniel E Freedberg (DE)

Department of Medicine, Columbia University Irving Medical Center, New York, New York.

Hossein Khiabanian (H)

Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, New Jersey.

Yael R Nobel (YR)

Department of Medicine, Columbia University Irving Medical Center, New York, New York.

Stephania Stump (S)

Department of Medicine, Columbia University Irving Medical Center, New York, New York.
Microbiome Core Facility, Columbia University Irving Medical Center, New York, New York.

Anne-Catrin Uhlemann (AC)

Department of Medicine, Columbia University Irving Medical Center, New York, New York.
Microbiome Core Facility, Columbia University Irving Medical Center, New York, New York.

Charles J Lightdale (CJ)

Department of Medicine, Columbia University Irving Medical Center, New York, New York.

Julian A Abrams (JA)

Department of Medicine, Columbia University Irving Medical Center, New York, New York. ja660@cumc.columbia.edu.

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Classifications MeSH