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Drinking from the fountain of promise: biomarkers in the surveillance of Barrett’s oesophagus—the glass is half full!
  1. S L Preston1,
  2. J A Jankowski2
  1. 1Department of Gastroenterology, Concord Repatriation General Hospital, Sydney, Australia, and Histopathology Unit, Cancer Research UK, London, UK
  2. 2Department 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
  1. Correspondence to:
    Professor J A Jankowski
    Department of Clinical Pharmacology, University of Oxford, Woodstock Rd, Oxford OX2 6HE, UK; janusz.jankowski{at}

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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

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 natural history of the adenoma:carcinoma sequence in the colon has translated to clinical medicine, prompting the removal of adenomatous polyps at the premalignant stage, with an associated reduction in the incidence of colorectal cancer.6,7 Regrettably, thus far, such gains have not been made in dysplasia in the context of BO, with the effectiveness of current surveillance strategies yet to be conclusively proven; a matter soon to be addressed by the BOSS (Barrett’s Oesophagus Surveillance Study), a study integrated with the AspECT (Aspirin and Esomprazole Chemoprevention Trial of Cancer in Barrett’s Oesophagus) (7500 patients in total).8 At present, a patient with BO can only be risk stratified on the basis of either …

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  • Conflict of interest: None declared.

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