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Gut 2006;55:1377-1379; doi:10.1136/gut.2006.096461
Copyright © 2006 BMJ Publishing Group Ltd & British Society of Gastroenterology.

COMMENTARY

Oesophagus

Drinking from the fountain of promise: biomarkers in the surveillance of Barrett’s oesophagus—the glass is half full!

S L Preston1, J A Jankowski2

1 Department of Gastroenterology, Concord Repatriation General Hospital, Sydney, Australia, and Histopathology Unit, Cancer Research UK, London, UK
2 Department of Clinical Pharmacology, University of Oxford, Oxford, UK, Digestive Diseases Centre, University Hospitals of Leicester, Leicester, UK, and Histopathology Unit, Cancer Research UK, London, UK

Correspondence to:
Correspondence to:
Professor J A Jankowski
Department of Clinical Pharmacology, University of Oxford, Woodstock Rd, Oxford OX2 6HE, UK; janusz.jankowski@clinpharm.ox.ac.uk


Biomarkers for prognostication need large randomised controlled trials such as AspECT and BOSS. These trials will deliver surrogates which fulfil the validation criteria necessary for their introduction into the clinic

Keywords: biomarkers; Barrett’s oesophagus; oesophageal cancer; stem cells

The first 150 words of the full text of this article appear below.

Barrett’s oesophagus (BO) is an acquired premaligant condition that is the only known precursor to oesophageal adenocarcinoma (OA); a malignancy whose incidence has risen steadily in the Western world in the last 20–30 years.1 The lifetime risk of developing an adenocarcinoma in the context of BO is 2–5%,2 and despite recent advances in its treatment the associated morbidity and mortality remain high.3 BO advances through a series of morphological stages: from metaplasia through dysplasia of different grades and finally to adenocarcinoma—the metaplasia-dysplasia-adenocarcinoma sequence (MCS).4,5 Although this genetic process is not as well outlined as in the colon,4 it is thought to be a similar multistep process consisting of genetic and epigenetic mutations, involving the same or a similar group of genes, which over many years leads to increasing genomic instability and ultimately to the formation of an autonomous clone of cells with invasive and metastatic properties.5

Knowledge of the . . . [Full text of this article]


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TP53 and progression from Barrett’s metaplasia to oesophageal adenocarcinoma in a UK population cohort
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