EditorialsCarcinogenesis at the gastroesophageal junction: Free radicals at the frontier☆,☆☆
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Cited by (33)
Chemoprevention in Barrett's Esophagus: Current Status
2015, Gastroenterology Clinics of North AmericaCitation Excerpt :A preclinical study conducted by us established that the use of selective and nonselective COX-2 inhibitors in a rodent model of chronic reflux produced a statistically significant reduction in relative risk of developing EAC by 55% in rats treated with MF-tricyclic and 79% (P<.01) in those treated with sulindac as compared with the control group. The degree of inflammation was found to be more severe in the control group compared with the study group.22 In summary, downregulation of PGE2 levels, either by KLF11-mediated inhibition of cPLA2α or through COX2 inhibition, reduces cell growth in vitro and neoplastic transformation in Barrett’s and mucosa of animals with reflux injury.24,25,28,29
Chemoprevention in Barrett's oesophagus
2015, Best Practice and Research: Clinical GastroenterologyCitation Excerpt :Oral microbes on the tongue reduce the salivary nitrates to nitrites [82]. When these nitrites come into contact with contents of gastro-duodenal reflux in the lower oesophagus, they change to nitrous acid that decomposes immediately into nitric oxide [83]. Nitric oxide is considered tumorigenic via DNA damage, lipid peroxidation and mutagenesis.
Esophageal adenocarcinoma arising in Barrett esophagus
2009, Cancer LettersCitation Excerpt :Following World War II, Western countries sharply increased their use of nitrate-based fertilizers, resulting in an increased concentration of nitrates in vegetables. It is conceivable that this has contributed to the rising frequency of esophageal adenocarcinoma [11,12]. Despite this attractive theory, the bulk of available epidemiological data suggest that a diet high in fruits and vegetables may protect against Barrett and adenocarcinoma of the esophagus.
Nitric Oxide and Acid Induce Double-Strand DNA Breaks in Barrett's Esophagus Carcinogenesis via Distinct Mechanisms
2007, GastroenterologyCitation Excerpt :In addition, we showed for the first time that acid can induce double-strand DNA breaks in these same esophageal cell lines and that this is mediated by intracellular production of ROS. Our data provide a mechanistic rationale for previously proposed hypotheses linking increased nitrate intake because of use of nitrogen-based fertilizers50 or economic status51 with trends in the incidence of EAC. This study also lends support to the idea that antioxidant therapy, other than vitamin C, may be an appropriate strategy in preventing the progression of BE to EAC.
Epidemiologic risk factors for Barrett's esophagus and associated adenocarcinoma
2005, Clinical Gastroenterology and HepatologyBarrett's esophagus
2004, Journal of Gastrointestinal Surgery
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Address requests for reprints to: Stuart Jon Spechler, M.D., Chief, Division of Gastroenterology (111B1), Dallas VA Medical Center, 4500 South Lancaster Road, Dallas, Texas 75216. e-mail: [email protected]; Fax: (214) 857-1571.
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Supported by Astra Zeneca and Wyeth-Ayerst. The author is a consultant for Astra Zeneca, TAP, and Janssen.