Commentaries
Epigenetic changes wipe out protective mechanisms in Barrett’s oesophagus
Correspondence to:
Dr Rebecca Fitzgerald, MRC Cancer Cell Unit, Hutchison-MRC Research Centre, Cambridge, CB22 0XZ; rcf@hutchison-mrc.cam.ac.uk
| The first 150 words of the full text of this article appear below. |
Reactive oxygen and nitrogen species play important roles in the regulation of cell survival. The effects are dose dependent and consist of two stages: reversible redox regulation and irreversible oxidative molecular damage. The Barrett’s oesophageal epithelium is bathed in a hostile luminal environment comprising reflux and dietary components. Increasing evidence suggests that these factors lead to abnormal levels of oxidative stress in the metaplastic epithelium, thus setting the stage for dysplasia and adenocarcinoma1–4 Cancer might seem inevitable in the face of such insults but, due to a plethora of defence mechanisms, this outcome is usually avoided. Although the mechanisms by which higher organisms respond to elevated oxygen and nitrogen species in vivo is poorly understood, the endogenous antioxidases are a key mechanism through which our cells combat oxidative stress. Key enzyme families include the glutathione S-transferases and peroxidases, and the loci encoding these enzymes comprise large supergene families. The
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
Relevant Article
- DNA hypermethylation regulates the expression of members of the Mu-class glutathione S-transferases and glutathione peroxidases in Barrett’s adenocarcinoma
- D F Peng, M Razvi, H Chen, K Washington, A Roessner, R Schneider-Stock, and W El-Rifai
Gut 2009 58: 5-15.[Abstract] [Full Text] [PDF]
- Full Text
- Full Text (PDF)
- Alert me when this article is cited
- Alert me if a correction is posted
- Citation Map
Services
- Email this link to a friend
- Similar articles in this journal
- Similar articles in PubMed
- Add article to my folders
- Download to citation manager
- Request Permissions
Citing Articles
Google Scholar
PubMed
Topic Collections
Bookmark with
Register for free content
The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.
Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.
