Frequent Occurrence of Mitochondrial DNA Mutations in Barrett’s Metaplasia without the Presence of Dysplasia

Lee, Soong; Han, Moon-jong; Lee, Ki-Sang; Back, Seung-Chul; Hwang, David; Kim, Hwan-Young; Shin, Jong‐Hee; Suh, Soon Pal; Ryang, Dong‐Wook; Kim, Hye‐Ran; Shin, Myung‐Geun

doi:10.1371/journal.pone.0037571

Cited by 13 publications

(16 citation statements)

References 23 publications

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“…Mitochondrial DNA mutations have been reported in EA, BE and cell cultures derived from BE 117–120 . No large scale studies have been reported in either BE or EA, and their role in progression is currently unknown.…”

Section: Genomic Evolution Of Ea and Bementioning

confidence: 99%

Genetic Insights in Barrett’s Esophagus and Esophageal Adenocarcinoma

Reid

Paulson

2015

Gastroenterology

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Beginning in the 1980s, an alarming rise in the incidence of esophageal adenocarcinoma (EA) led to screening of patients with reflux to detect Barrett’s esophagus (BE) and surveillance of BE to detect early EA. This strategy, based on linear progression disease models, resulted in selective detection of BE that does not progress to EA over a lifetime (overdiagnosis) and missed BE that rapidly progresses to EA (underdiagnosis). Here we review the historical thought processes that resulted in this undesired outcome and the transformation in our understanding of genetic and evolutionary principles governing neoplastic progression that has come from application of modern genomic technologies to cancers and their precursors. This new synthesis provides improved strategies for prevention and early detection of EA by addressing the environmental and mutational processes that can determine “windows of opportunity” in time to detect rapidly progressing BE and distinguish it from slowly or non-progressing BE.

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Section: Genomic Evolution Of Ea and Bementioning

confidence: 99%

Genetic Insights in Barrett’s Esophagus and Esophageal Adenocarcinoma

Reid

Paulson

2015

Gastroenterology

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“…This suggest possible role of the mtDNA in progression of the IM into dysplasia. [54, 55]. In another prospective cohort study, selenoprotein P concentration was found to be positively correlated with risk of EAC with hazard ratio of 3.95 but not the serum selenium concentration.…”

Section: Surveillancementioning

confidence: 99%

Barrett’s Esophagus in 2012: Updates in Pathogenesis, Treatment, and Surveillance

Chandra

Gorospe

Leggett

et al. 2013

Curr Gastroenterol Rep

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Barrett’s esophagus (BE) is the only established precursor lesion in the development of esophageal adenocarcinoma (EAC) and increases the risk of cancer by eleven fold. It is regarded as a complication of gastroesophageal reflux disease. There is ever increasing body of knowledge on the pathogenesis, diagnosis, treatment and surveillance of BE and its associated dysplasia. In this review, we summarize the latest advances in BE research and clinical practice in the past 2 years. It is critical to understand both the molecular underpinnings of this disorder to comprehend the clinical outcomes of the disease. For clinical gastroenterologists, there is also continuous growth of endoscopic approaches is daunting and further improvements in the detection and treatment of BE and early EAC are anticipated. In the future, we may see the increased role of biomarkers, both molecular and imaging, in both diagnostic and therapeutic strategies for BE.

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“…Although for the majority of identified genes, the predictive or prognostic value remains unclear. Nearly all of the new markers have not yet been validated in prospective controlled or randomized studies [ 30 ].…”

Section: Mtdna Aberrations In Chronic Inflammatory Diseasesmentioning

confidence: 99%

Mitochondrial DNA Aberrations and Pathophysiological Implications in Hematopoietic Diseases, Chronic Inflammatory Diseases, and Cancers

et al. 2015

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Mitochondria are important intracellular organelles that produce energy for cellular development, differentiation, and growth. Mitochondrial DNA (mtDNA) presents a 10- to 20-fold higher susceptibility to genetic mutations owing to the lack of introns and histone proteins. The mtDNA repair system is relatively inefficient, rendering it vulnerable to reactive oxygen species (ROS) produced during ATP synthesis within the mitochondria, which can then target the mtDNA. Under conditions of chronic inflammation and excess stress, increased ROS production can overwhelm the antioxidant system, resulting in mtDNA damage. This paper reviews recent literature describing the pathophysiological implications of oxidative stress, mitochondrial dysfunction, and mitochondrial genome aberrations in aging hematopoietic stem cells, bone marrow failure syndromes, hematological malignancies, solid organ cancers, chronic inflammatory diseases, and other diseases caused by exposure to environmental hazards.

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Frequent Occurrence of Mitochondrial DNA Mutations in Barrett’s Metaplasia without the Presence of Dysplasia

Cited by 13 publications

References 23 publications

Genetic Insights in Barrett’s Esophagus and Esophageal Adenocarcinoma

Genetic Insights in Barrett’s Esophagus and Esophageal Adenocarcinoma

Barrett’s Esophagus in 2012: Updates in Pathogenesis, Treatment, and Surveillance

Mitochondrial DNA Aberrations and Pathophysiological Implications in Hematopoietic Diseases, Chronic Inflammatory Diseases, and Cancers

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