Research Papers: GastrointestinalAspirin is not chemoprotective for Barrett's adenocarcinoma of the oesophagus in multicentre cohortGatenby, Piers A.; Ramus, James R.; Caygill, Christine P.; Winslet, Marc C.; Watson, Anthony Author Information UK National Barrett's Oesophagus Registry (UKBOR), Division of Surgical and Interventional Science, University College London, London, UK Correspondence to Piers A. Gatenby, MA, MD, MRCS, UK National Barrett's Oesophagus Registry (UKBOR), Division of Surgical and Interventional Science, University College London, Royal Free Campus, Rowland Hill Street, London NW3 2PF, UK Tel: +44 20 7472 6223; fax: +44 20 7472 6224; e-mail: [email protected] Received 22 April 2009 Accepted 22 April 2009 European Journal of Cancer Prevention: September 2009 - Volume 18 - Issue 5 - p 381-384 doi: 10.1097/CEJ.0b013e32832e0955 Buy Metrics Abstract Barrett's columnar-lined oesophagus is the precursor lesion for oesophageal adenocarcinoma. The overall rate of progression to adenocarcinoma is 0.59% per annum. A large prospective multicentre trial is recruiting to assess the role of aspirin as a chemoprotective agent in prevention of development of cancer as well as cardiovascular protection in patients with Barrett's oesophagus. This retrospective analysis of the large UK National Barrett's Oesophagus Registry database seeks to analyse this question from within its large natural history study cohort. Multicentre UK retrospective cohort compared patients known to have been taking aspirin with those who did not take aspirin during the course of surveillance for columnar-lined oesophagus. End point was development of dysplasia or oesophageal adenocarcinoma. Analysis was undertaken using Cox's proportional hazard ratio. Total follow-up was 3683 patient-years. Eighty-six patients were taking aspirin, 650 were not taking aspirin (reference group). Numbers of patients developing all grades of dysplasia and adenocarcinoma were: 13 aspirin (15.1%) and 97 no aspirin (14.9%) (hazard ratio 0.723, 95% confidence interval 0.410–1.310, P = 0.294), high-grade dysplasia and adenocarcinoma: five aspirin (5.8%) and 25 no aspirin (3.8%) (hazard ratio 0.898, 95% confidence interval 0.340–2.368, P = 0.827) and adenocarcinoma: four aspirin (4.7%) and 16 no aspirin (2.5%) (hazard ratio 1.092, 95% confidence interval 0.358–3.335, P = 0.877). No significant difference was observed in hazard of developing dysplasia or adenocarcinoma between patients taking aspirin and those not taking aspirin during the course of follow-up of surveillance for columnar-lined oesophagus. In conclusion, no difference in risk of development of dysplasia or adenocarcinoma was observed between patients taking aspirin and those not taking aspirin in this large cohort. © 2009 Lippincott Williams & Wilkins, Inc.