Potential Role of the Microbiome in Barrett’s Esophagus and Esophageal Adenocarcinoma

Snider, Erik J.; Freedberg, Daniel E.; Abrams, Julian A.

doi:10.1007/s10620-016-4155-9

Cited by 64 publications

(58 citation statements)

References 71 publications

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“…Changes in the composition of esophageal microorganisms can damage the esophageal mucosal barrier, leading to mucosal inflammation and persistent disease . Although we found that the composition of esophageal microbiota differed between controls and patients with RE, we were unable to determine the causal relationship between changes in the microbiota composition and RE …”

Section: Discussionmentioning

confidence: 71%

“…9,10 Although we found that the composition of esophageal microbiota differed between controls and patients with RE, we were unable to determine the causal relationship between changes in the microbiota composition and RE. 25 Research has suggested that a high prevalence of Helicobacter pylori (H. pylori) infection in Asians could protect them against GERD. 26 The protective effects of H. pylori infection may be related to its negative effect on the secretion of gastric acid and the production of ghrelin, a hormone in the gastrointestinal tract that stimulates appetite.…”

Section: Discussionmentioning

confidence: 99%

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Changes in the distal esophageal microbiota in Chinese patients with reflux esophagitis

Gao

Chen

et al. 2018

J of Digest Diseases

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Objective Changes in microbiota composition in the distal esophagus may be associated with the pathogenesis of gastroesophageal reflux disease. We aimed to compare the composition of distal esophageal microbiota between Chinese patients with reflux esophagitis (RE) and healthy volunteers using metagenomic high‐throughput DNA sequencing and bioinformatic analyses. Methods Healthy volunteers (controls) and patients with reflux esophagitis (RE) were enrolled. Distal esophageal (2 cm above the gastroesophageal junction) biopsy specimens were obtained under endoscopy. Microbial DNA was extracted from the specimens, followed by 16S rDNA gene amplification and Illumina sequencing. Bioinformatic tools were applied to dissect the community structure. Results No dramatic differences in microbiota were found in RE patients compared with the controls. At the phylum level, only Bacteroidetes differed between the groups, being less abundant in the RE group. The overall number and diversity of species tended to be lower in RE patients, but there were no significant differences between the groups. Three genera, Prevotella, Helicobacter, and Moraxella, were obviously depleted in RE patients, as revealed by linear discriminant analysis. Conclusions The composition of distal esophageal microbiota in Chinese patients with RE showed moderate changes compared with healthy controls. To what extent these changes are associated with the pathogenesis of RE needs further investigation.

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Changes in the distal esophageal microbiota in Chinese patients with reflux esophagitis

Gao

Chen

et al. 2018

J of Digest Diseases

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Section: Introductionmentioning

confidence: 99%

“…Esophageal adenocarcinoma (EAC) has increased greater than 10‐fold over recent decades . Unfortunately, the overall 5‐year survival of patients with EAC is below 19%, with most tumors discovered in advanced stages, after local invasion and/or metastasis occurred . Most EACs arise in patients with Barrett's esophagus (BE), which is characterized by replacement of the normal squamous esophageal mucosa by columnar epithelium with intestinal metaplasia (IM) and may subsequently progress to dysplasia and adenocarcinoma (DAC), through progressive development of low‐grade dysplasia (LGD), high‐grade dysplasia (HGD), intramucosal adenocarcinoma and advanced adenocarcinoma …”

Section: Introductionmentioning

confidence: 99%

“…[1][2][3][4][5] Unfortunately, the overall 5-year survival of patients with EAC is below 19%, 6 with most tumors discovered in advanced stages, after local invasion and/or metastasis occurred. 2,3 Most EACs arise in patients with Barrett's esophagus (BE), 7 which is characterized by replacement of the normal squamous esophageal mucosa by columnar epithelium with intestinal metaplasia (IM) and may subsequently progress to dysplasia and adenocarcinoma (DAC), through progressive development of low-grade dysplasia (LGD), high-grade dysplasia (HGD), intramucosal adenocarcinoma and advanced adenocarcinoma. 8 Established factors for increased risk of BE and EAC include older age, male sex, white ethnic, gastroesophageal reflux, smoking and obesity, whereas gastric H. pylori infection is associated with a decreased risk.…”

Section: Introductionmentioning

confidence: 99%

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High‐resolution genomic alterations in Barrett's metaplasia of patients who progress to esophageal dysplasia and adenocarcinoma

Sepulveda

Komissarova

Kongkarnka

et al. 2019

Intl Journal of Cancer

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The main risk factor for esophageal dysplasia and adenocarcinoma (DAC) is Barrett's esophagus (BE), characterized by intestinal metaplasia. The critical genomic mechanisms that lead to progression of nondysplastic BE to DAC remain poorly understood and require analyses of longitudinal patient cohorts and high‐resolution assays. We tested BE tissues from 74 patients, including 42 nonprogressors from two separate groups of 21 patients each and 32 progressors (16 in a longitudinal cohort before DAC/preprogression‐BE and 16 with temporally concurrent but spatially separate DAC/concurrent‐BE). We interrogated genome‐wide somatic copy number alterations (SCNAs) at the exon level with high‐resolution SNP arrays in DNA from formalin‐fixed samples histologically confirmed as nondysplastic BE. The most frequent abnormalities were SCNAs involving FHIT exon 5, CDKN2A/B or both in 88% longitudinal BE progressors to DAC vs. 24% in both nonprogressor groups (p = 0.0004). Deletions in other genomic regions were found in 56% of preprogression‐BE but only in one nonprogressor‐BE (p = 0.0004). SCNAs involving FHIT exon 5 and CDKN2A/B were also frequently detected in BE temporally concurrent with DAC. TP53 losses were detected in concurrent‐BE but not earlier in preprogression‐BE tissues of patients who developed DAC. CDKN2A/p16 immunohistochemistry showed significant loss of expression in BE of progressors vs. nonprogressors, supporting the genomic data. Our data suggest a role for CDKN2A/B and FHIT in early progression of BE to dysplasia and adenocarcinoma that warrants future mechanistic research. Alterations in CDKN2A/B and FHIT by high‐resolution assays may serve as biomarkers of increased risk of progression to DAC when detected in BE tissues.

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Cystic fibrosis and fat malabsorption: Pathophysiology of the cystic fibrosis gastrointestinal tract and the impact of highly effective CFTR modulator therapy

McDonald,

Reid,

Pohl

et al. 2024

Nut in Clin Prac

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Cystic fibrosis (CF) is a progressive, genetic, multi‐organ disease affecting the respiratory, digestive, endocrine, and reproductive systems. CF can affect any aspect of the gastrointestinal (GI) tract, including the esophagus, stomach, small intestine, colon, pancreas, liver, and gall bladder. GI pathophysiology associated with CF results from CF membrane conductance regulator (CFTR) dysfunction. The majority of people with CF (pwCF) experience exocrine pancreatic insufficiency resulting in malabsorption of nutrients and malnutrition. Additionally, other factors can cause or worsen fat malabsorption, including the potential for short gut syndrome with a history of meconium ileus, hepatobiliary diseases, and disrupted intraluminal factors, such as inadequate bile salts, abnormal pH, intestinal microbiome changes, and small intestinal bacterial overgrowth. Signs and symptoms associated with fat malabsorption, such as abdominal pain, bloating, malodorous flatus, gastroesophageal reflux, nausea, anorexia, steatorrhea, constipation, and distal intestinal obstruction syndrome, are seen in pwCF despite the use of pancreatic enzyme replacement therapy. Given the association of poor nutrition status with lung function decline and increased mortality, aggressive nutrition support is essential in CF care to optimize growth in children and to achieve and maintain a healthy body mass index in adults. The introduction of highly effective CFTR modulator therapy and other advances in CF care have profoundly changed the course of CF management. However, GI symptoms in some pwCF may persist. The use of current knowledge of the pathophysiology of the CF GI tract as well as appropriate, individualized management of GI symptoms continue to be integral components of care for pwCF.

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Potential Role of the Microbiome in Barrett’s Esophagus and Esophageal Adenocarcinoma

Cited by 64 publications

References 71 publications

Changes in the distal esophageal microbiota in Chinese patients with reflux esophagitis

Changes in the distal esophageal microbiota in Chinese patients with reflux esophagitis

High‐resolution genomic alterations in Barrett's metaplasia of patients who progress to esophageal dysplasia and adenocarcinoma

Cystic fibrosis and fat malabsorption: Pathophysiology of the cystic fibrosis gastrointestinal tract and the impact of highly effective CFTR modulator therapy

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