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BSG Inflammatory Bowel Disease Symposium Pathology Free Papers BSG abstracts BSG inflammatory bowel disease symposium resetting immune responses and by other mechanisms, autologous stem cell transplantation has the potential to cure Crohn’s disease. O-01 DIETARY DOCOSAHEXAENOIC ACID REDUCES THE RISK OF Case reports suggest this is the case for some but not all patients. DEVELOPING ULCERATIVE COLITIS – A MULTI-CENTRE Aims and Methods: The ASTIC Trial randomises patients with EUROPEAN PROSPECTIVE COHORT STUDY poor quality of life despite 3 immunosuppressive agents to undergo Gut: first published as on 23 March 2009. Downloaded from stem cell mobilisation followed by ablation and transplantation AR Hart for The IBD in EPIC Study Investigators. School of Medicine, University of East immediately or after 1 year, and compares the number in drug free Anglia, Norwich, UK clinical and endoscopic remission at the end of 1 year. Results: Eighteen patients have been considered by the Steering Introduction: Dietary docosahexaenoic acid (DHA), an n-3 Committee. Eight have been approved unconditionally and five polyunsaturated fatty acid obtained principally from fish, has subject to specific improvements in health or management. Nine anti-inflammatory effects on many cellular processes, and may patients who have entered the study are shown in the table. Four prevent the development of ulcerative colitis. Currently, there are patients did not proceed to trial entry because of spontaneous no prospective epidemiological data from multicentre studies improvements. As at November 1 2008, 4 serious adverse events investigating this hypothesis. have been reported (3 infective, 3 serious, 1 SUSARs). Data on Aims and Methods: The aim was to examine the prospective efficacy will be analysed on March 1 2009 and will be presented. relationship between the dietary intake of DHA and the develop- Conclusion: There are a significant number of patients with ment of ulcerative colitis in participants enrolled in a large European Crohn’s disease for whom stem cell transplantation is an appro- cohort study. The populations comprised 189 610 men and women, priate course of action. The main risks are related to infection. aged 30–74 years, participating in a cohort study (EPIC European Prospective Investigation Into Cancer & Nutrition). Participants were resident in either the UK, Sweden, Denmark or Germany. They provided information on diet at recruitment, by completing food frequency questionnaires, and were followed up for the Pathology free papers diagnosis of ulcerative colitis. Each incident case was matched with four controls and the intake of DHA divided into quartiles. The O-03 DOES THE ECTOPIC EXPRESSION OF CDX2 PROVOKE analysis was performed using logistic regression adjusted for gender, EXPRESSION OF INTESTINAL GENES IN OESOPHAGEAL age, total energy intake, smoking, centre and other fatty acids CELLS? http://gut.bmj.com/ which affect DHA formation. 1BJ Colleypriest, 2JM Farrant, 1D Tosh, 1JMW Slack. 1Biology and Biochemistry, Results: A total of 118, initially healthy participants, developed University of Bath, UK; 2Gastroenterology, Royal United Hospital, Bath, UK ulcerative colitis (53 women, 65 men) after a median follow-up time of 4.0 years (range 1.7–11.3 years). The odds ratio for the highest Introduction: Oesophageal adenocarcinoma and its precursor versus the lowest quartile of intake of DHA acid was 0.24 (95% CI lesion, Barrett’s metaplasia, are both exhibiting a rapidly increasing 0.06 to 0.99). incidence. Whilst many of the molecular mechanisms in the Conclusion: These results, together with plausible biological progression from Barrett’s metaplasia to cancer are understood mechanisms, support the hypothesis that dietary DHA may reduce the initial step to intestinal metaplasia is not. The transcription on September 26, 2021 by guest. Protected copyright. the risk of developing ulcerative colitis. Further epidemiological factor caudal type homeobox transcription factors 2 (cdx2) has been studies are needed to investigate this finding, which if confirmed, implicated in the pathogenesis of Barrett’s. The expression of cdx2 has implications for the prevention of ulcerative colitis. If the is normally limited to the post pyloric epithelium of the association is causal then increasing the population’s intake of DHA gastrointestinal tract, but it is present in Barrett’s tissue. may prevent 30% of cases of ulcerative colitis. Transgenic studies have demonstrated that ectopic expression of cdx2 in the gastric mucosa results in ectopic intestinal tissue; this has not however been demonstrated in oesophageal tissue. We O-02 AUTOLOGOUS STEM CELL TRANSPLANTATION FOR CROHN’S present a novel long term in vitro model of squamous mouse DISEASE (ASTIC) TRIAL: EARLY REPORT OF TOXICITY AND oesophagus which recapitulate the full repertoire of cell phenotypes EFFICACY found in the oesophagus. We have investigated the result of ectopic CJ Hawkey. Nottingham Digestive Diseases Centre and Biomedical Research Unit, cdx2 expression within this model. Nottingham University Hospital, Nottingham, UK Aims and Methods: Explants of mouse oesophageal epithelium are cultured and characterised using immunofluorescent immuno- Introduction: Some patients with Crohn’s disease are resistant to histochemistry. Transgenes are expressed within the explant available treatments and these control but do not cure the disease. By culture using recombinant adenovirus such as ad-cmv-GFP and ad-cmv-cdx2. Changes in gene expression, particularly the induc- tion of intestinal genes, are assessed by PCR. Abstract 02 Results: The explant culture system is viable in culture for over 6 months. There is a connective tissue and epithelial components, Age Sex Duration Montreal Surgery Status as demonstrated by smooth muscle actin and e-cadherin expressing 23 M 9 years A1L3L4B2p 0 Transplant cells, within the culture. The epithelial cells within the model 23 F 12 years A1L3L4B3p 9 Transplant express markers of full stratification; cytokeratins 5, 14 and 4, 33 F 7 years A2L1B2 0 Withdrawn involucrin and loricrin as well as the squamous transcription factor 39 M 17 years A2L3B1p 2 Transplant p63. Incubation with recombinant adenovirus, ad-cmv-cdx2 results 36 M 15 years A2L3B1 0 Mobilised in epithelial expression of cdx2 protein assessed by immunofluor- 29 F 15 years A2L2B1 0 Baseline escence. The ectopic expression of cdx2 within the epithelium of 22 F 3 years A1L3L4B1 0 Baseline this model does not promote the transcription of any intestinal 44 F 15 years A2L4B1p 4 Baseline genes. Mucin 2, sucrose isomaltase, lactase phlorizin, alkaline 26 F 10 years A1L4B2p 2 Mobilised phosphatase, trefoil factor 3, villin, chromogranin A and cryptdin 1 were all looked for using PCR. Gut 2009;58(Suppl I):A1–A156 A1 BSG abstracts Conclusion: The long-term in vitro model of squamous oesopha- crypts. Methylation of the CpG islands of some non-expressed gus recapitulates the full repertoire of oesophageal cells found in genes has been shown to be a useful clonal marker to study cell vivo. Ectopic gene expression, and the effects thereof, is possible turnover within crypts.12 However, doubt remains about the using adenoviral vectors. Cdx2 expression within oesophageal efficacy of methylation as a clonal marker to investigate expansion squamous cells does not result in the expression of intestinal genes. of the crypts themselves. However, despite this uncertainty, These findings contrast with previous studies in gastric mucosa methylation patterns are used to study clonality throughout the suggesting that other factors are necessary in the oesophageal cells. gastrointestinal tract. Recently, we have shown that mitochondrial Gut: first published as on 23 March 2009. Downloaded from DNA (mtDNA) mutations provide an excellent method to 3 O-04 HUMAN SMALL INTESTINAL CRYPTS ARE CLONAL, CONTAIN investigate clonal expansion of colonic crypts. Patches of adjacent MULTIPLE STEM CELLS AND MUTATED CRYPTS DIVIDE BY mutated crypts, deficient in the mitochondrially encoded enzyme FISSION cytochrome-c-oxidase, are frequently observed: these patches form through repeated rounds of fission of the original mutated crypt. 1 1 1 1 2 2 L Gutierrez-Gonzalez, MDeheragoda, SJ Leedham, GElia, A Shankar, C Imber, Mutated crypts share the exact same mtDNA mutation, confirming 3DM Turnbull, 4M Novelli, 5JA Jankowski, 6NW Wright, 5SAC McDonald. 1Histopathology their shared ancestry. Here, we have investigated whether Unit, Cancer Research UK, London, UK; 2Surgery, University College London Hospitals, London, UK; 3School of Neurology, Neurobiology and Psychiatry, University of Newcastle methylation patterns can reveal the shared ancestry of crypts that upon Tyne, Newcastle upon Tyne, UK; 4Histopathology, University College London have been shown to be related by mtDNA. We considered how the Hospitals, UK; 5Centre for Gastroenterology, London, UK; 6Institute of Cell and Molecular dynamics of stem cell division may cause the methylation patterns Sciences, Barts and the London School of Medicine and Dentistry, London, UK of two related crypts to diverge. Aims and Methods: Serial sections of normal colonic mucosa were Introduction: Little is known about the clonal structure or stem cell histochemically stained for cytochrome-c-oxidase activity. A second architecture of human small intestinal crypts and how mutations stain for succinate dehydrogenase activity was used to highlight spread through the small bowel. Data from our laboratory, using cytochrome-c-oxidase deficiency. Crypt relatedness was confirmed
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