ArticlePloS one2012
Frequent occurrence of mitochondrial DNA mutations in Barrett's metaplasia without the presence of dysplasia.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Clonal Transitions and Phenotypic Evolution in Barrett's Esophagus.Gastroenterology · 2022Article
- Differential Expression Profiles of Oxidative Stress Levels, 8-oxo-dG and 4-HNE, in Barrett's Esophagus Compared to Esophageal Adenocarcinoma.International journal of molecular sciences · 2019Article
- Role of Mitochondrial Markers in Improved Detection and Risk-Stratification in Barrett's Esophagus Patients.The Yale journal of biology and medicine · 2019Review
- From genetics to signaling pathways: molecular pathogenesis of esophageal adenocarcinoma.Biochimica et biophysica acta. Reviews on cancer · 2019Review
- Precancer Atlas to Drive Precision Prevention Trials.Cancer research · 2017Article
- Changes in mitochondrial stability during the progression of the Barrett's esophagus disease sequence.BMC cancer · 2016Article
- Genetic Insights in Barrett's Esophagus and Esophageal Adenocarcinoma.Gastroenterology · 2015Review
- Mitochondrial DNA aberrations and pathophysiological implications in hematopoietic diseases, chronic inflammatory diseases, and cancers.Annals of laboratory medicine · 2015Review
- Biomarkers of Barrett's esophagus.World journal of gastrointestinal pathophysiology · 2014Review
- Predictive biomarkers for Barrett's esophagus: so near and yet so far.Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus · 2013Review
- Barrett's esophagus in 2012: updates in pathogenesis, treatment, and surveillance.Current gastroenterology reports · 2013Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBarrett's esophagus (BE) is one of the most common premalignant lesions and can progress to esophageal adenocarcinoma (EA). The numerous molecular events may play a role in the neoplastic transformation of Barrett's mucosa such as the change of DNA ploidy, p53 mutation and alteration of adhesion molecules. However, the molecular mechanism of the progression of BE to EA remains unclear and most studies of mitochondrial DNA (mtDNA) mutations in BE have performed on BE with the presence of dysplasia. METHODS/
findingsThus, the current study is to investigate new molecular events (Barrett's esophageal tissue-specific-mtDNA alterations/instabilities) in mitochondrial genome and causative factors for their alterations using the corresponding adjacent normal mucosal tissue (NT) and tissue (BT) from 34 patients having Barrett's metaplasia without the presence of dysplasia. Eighteen patients (53%) exhibited mtDNA mutations which were not found in adjacent NT. mtDNA copy number was about 3 times higher in BT than in adjacent NT. The activity of the mitochondrial respiratory chain enzyme complexes in tissues from Barrett's metaplasia without the presence of dysplasia was impaired. Reactive oxygen species (ROS) level in BT was significantly higher than those in corresponding samples. CONCLUSION/SIGNIFICANCE: High ROS level in BT may contribute to the development of mtDNA mutations, which may play a crucial role in disease progression and tumorigenesis in BE.
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