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DOI 10.1111/j.1365-2036.2006.03119.x

Медицинская библиотека · Alimentary pharmacology & therapeutics · 2006

Systematic review: Cyclo-oxygenase-2 in human oesophageal adenocarcinogenesis.

Mehta S, Boddy A, Johnson I T, Rhodes M

СтатьяСистематический обзорПеревод пока не подготовлен

Аннотация

BACKGROUND

Published in vitro and animal in vivo studies have demonstrated that cyclo-oxygenase-2 plays an important role during oesophageal adenocarcinogenesis. However, the extent to which these studies are directly relevant to events in the human lower oesophagus is questionable.

AIM: To perform a systematic review of all available human studies that have evaluated levels of cyclo-oxygenase-2 expression during the progression from Barrett's metaplasia to oesophageal adenocarcinoma.

METHODS

A literature search was performed to identify all studies which qualitatively or quantitatively assessed cyclo-oxygenase-2 protein or gene expression in either Barrett's, dysplastic or adenocarcinoma tissue in humans.

RESULTS

A total of 27 studies met the inclusion criteria. There was general agreement that cyclo-oxygenase-2 was either absent or very weakly expressed in normal oesophageal squamous mucosa, but considerable disagreement regarding the presence of cyclo-oxygenase-2 in Barrett's and low-grade dysplasia. All studies agreed that high-grade dysplasia and adenocarcinoma expressed cyclo-oxygenase-2 to some extent although levels varied considerably between tissue samples.

CONCLUSIONS

There is conflicting evidence in the literature for cyclo-oxygenase-2 playing an important role in early oesophageal adenocarcinogenesis. Other non-cyclo-oxygenase-2 targets may account for the epidemiological data supporting the use of non-steroidal anti-inflammatory drugs in the chemoprevention of oesophageal adenocarcinoma.

Для цитирования: Mehta S, Boddy A, Johnson I T, Rhodes M. Systematic review: Cyclo-oxygenase-2 in human oesophageal adenocarcinogenesis.. Alimentary pharmacology & therapeutics. 2006. DOI: 10.1111/j.1365-2036.2006.03119.x.

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