Review: Chemoprevention of esophageal adenocarcinoma

Abrams, Julian A.

doi:10.1177/1756283x08093568

Cited by 7 publications

(8 citation statements)

References 121 publications

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“…Other authors have reported that antioxidant supplements, such as vitamin C, may also be effective chemopreventive agents for Barrett's patients by protecting against the DCA-induced DNA damage and NF-κΒ activation [52]. The non-steroidal anti-inflammatory COX-2 inhibitors and the application of n-3 fatty acids could also play a chemopreventive role by suppressing the eicosanoid production as further investigators found out [66,67]. With such knowledge, perhaps a new therapy for patients with Barrett's esophagus to prevent the progression to esophageal adenocarcinoma may be the introduction of UDCA to alter the bile acid composition, in combination with the antioxidant vitamin C, COX-2 inhibitors or n-3 fatty acids.…”

Section: The Role Of Acids and Bile Acids In Barrett's Esophagusmentioning

confidence: 95%

The Role of Bile Acids in the Neoplastic Progression of Barrett's Esophagus - A Short Representative Overview

et al. 2012

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Barrett's esophagus (BE) is an intestinal metaplasia of the distal esophagus in which squamous cells are replaced by a columnar epithelium. It is considered as a premalignant lesion, which can lead to esophageal adenocarcinoma, a very aggressive type of cancer, and can often be found in patients with gastro-esophageal reflux disease (GERD). In spite of the widespread use of acid-suppressing therapy with proton pump inhibitors, the incidence of adenocarcinoma has been steadily rising during the last 30 years. So, it can strongly be suggested that refluxed material other than acid might contribute to the progression of cancer within Barrett's esophagus. Along with gastric acid, bile acids enter the esophagus during an episode of reflux, and bile acids may be important in carcinogenesis. In their refluxates, patients with GERD and BE show high concentrations of the hydrophobic bile salt deoxycholic acid (DCA), which has cytotoxic effects and is able to induce DNA damage in different cell types. Other bile acids, like the hydrophilic urodeoxycholic acid (UDCA), have been therapeutically used to treat cholestatic liver diseases and to prevent colon carcinoma. This article reviews the effects of bile acids and points out new perceptions in the progression of Barrett's-associated carcinogenesis.

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Section: The Role Of Acids and Bile Acids In Barrett's Esophagusmentioning

confidence: 95%

The Role of Bile Acids in the Neoplastic Progression of Barrett's Esophagus - A Short Representative Overview

et al. 2012

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“…Recently, some chemical agents such as proton pump inhibitors (PPIs), nonsteroidal anti-inflammatory drugs (NSAIDs), selective cyclooxygenase-2 inhibitors (COXIBs), green tea, retinoic acid and thioproline have been reported to prevent EAC [22]. We performed several experiments by our rodent model using rabeprazole, thioproline or celecoxib to prevent inflammation-metaplasia-adenocarcinoma (IMA) sequence.…”

Section: Prevention Of Barrett Esophagus and Esophageal Adenocarcinomamentioning

confidence: 99%

Inflammation-Related Carcinogenesis and Prevention in Esophageal Adenocarcinoma Using Rat Duodenoesophageal Reflux Models

Fujimura

Oyama

Sasaki

et al. 2011

Cancers

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Development from chronic inflammation to Barrett's adenocarcinoma is known as one of the inflammation-related carcinogenesis routes. Gastroesophageal reflux disease induces regurgitant esophagitis, and esophageal mucosa is usually regenerated by squamous epithelium, but sometimes and somewhere replaced with metaplastic columnar epithelium. Specialized columnar epithelium, so-called Barrett's epithelium (BE), is a risk factor for dysplasia and adenocarcinoma in esophagus. Several experiments using rodent model inducing duodenogastroesophageal reflux or duodenoesophageal reflux revealed that columnar epithelium, first emerging at the proliferative zone, progresses to dysplasia and finally adenocarcinoma, and exogenous carcinogen is not necessary for cancer development. It is demonstrated that duodenal juice rather than gastric juice is essential to develop esophageal adenocarcinoma in not only rodent experiments, but also clinical studies. Antireflux surgery and chemoprevention by proton pump inhibitors, nonsteroidal anti-inflammatory drugs, selective cyclooxygenase-2 inhibitors, green tea, retinoic acid and thioproline showed preventive effects on the development of Barrett's adenocarcinoma in rodent models, but it remains controversial whether antireflux surgery could regress BE and prevent esophageal cancer in clinical observation. The Chemoprevention for Barrett's Esophagus Trial (CBET), a phase IIb, multicenter, randomized, double-masked study using celecoxib in patients with Barrett's dysplasia failed to prove to prevent progression of dysplasia to cancer. The AspECT (Aspirin Esomeprazole Chemoprevention Trial), a large multicenter phase III randomized trial to evaluate the effects of esomeprazole and/or aspirin on the rate of progression to high-grade dysplasia or adenocarcinoma in patients with BE is now ongoing.

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“…Accordingly, a number of in vitro and animal studies suggest a possible chemopreventive effect of COX-2 inhibitors in Barrett's mucosa [23] . Cultured cells from Barrett's epithelium, gained by endoscopic biopsies, and treated with a selective COX-2 inhibitor showed a significant decrease in COX-2 expression and in cell proliferation [24] .…”

Section: Nonsteroidal Anti-inflammatory Drugsmentioning

confidence: 99%

“…Male gender is an established risk factor for different diseases, including BE and associated adenocarcinoma, possibly due to the lack of the protective effect of estrogen and progesterone that is present in females [23] . However, population-based studies were not able to show a significant association of hormone replacement therapy with the risk of EAC [67,68] .…”

Section: Hormonesmentioning

confidence: 99%

Chemoprevention of Adenocarcinoma Associated with Barrett’s Esophagus: Potential Options

Neumann

Mönkemüller²,

Malfertheiner³

2009

Dig Dis

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Barrett’s esophagus (BE) is established as the primary precursor lesion of esophageal adenocarcinoma (EAC). The risk of esophageal cancer is 30–125 times greater compared to an age-matched population and survival rates are low, with only 15% of patients being alive 5 years after initial diagnosis. Therefore, surveillance strategies in BE are recommended to detect intraepithelial neoplasia and early carcinoma which in turn can be resected using endoscopic methods. Nevertheless, surveillance strategies have not had a major benefit in decreasing the incidence of EAC. Thus, attention should also be given to potential targets for prevention strategies that might arrest or delay the progression of BE to EAC. This article focuses on known and postulated targets for prevention of distal esophageal cancer.

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Review: Chemoprevention of esophageal adenocarcinoma

Cited by 7 publications

References 121 publications

The Role of Bile Acids in the Neoplastic Progression of Barrett's Esophagus - A Short Representative Overview

The Role of Bile Acids in the Neoplastic Progression of Barrett's Esophagus - A Short Representative Overview

Inflammation-Related Carcinogenesis and Prevention in Esophageal Adenocarcinoma Using Rat Duodenoesophageal Reflux Models

Chemoprevention of Adenocarcinoma Associated with Barrett’s Esophagus: Potential Options

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