RESUMO
Barrett's esophagus (BE) is the only known precursor of esophageal adenocarcinoma (EAC) and is amenable to treatment. However, more than 90 percent of EAC patients are never diagnosed with antecedent BE. Identification of molecular markers for BE is needed to improve detection of BE through efficient non-endoscopic methods that are cost-effective, sensitive and can be used to cater to a larger group of the population at risk. Alterations in mitochondria and mitochondrial DNA have been shown to be associated with various cancers, including esophageal cancer. Mitochondrial response to oxidative stress, alterations in mitochondrial metabolism, changes in mitochondrial membrane potential and mitochondrial genetic mutations have been found to be associated with BE pathogenesis. This mini-review focuses on the role of mitochondria in the pathogenesis of BE and EAC and the prospects of using that knowledge to develop effective strategies for the improved detection and risk-stratification in BE patients.
