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Title: Expression Analysis in Inflammatory Bowel Disease
P54
Hahn, Andreas(1); Costello, Christine(2); Lu, Tim(2); Lengauer, Thomas(3); Schreiber, Stefan(2)

Andreas.Hahn@scai.fraunhofer.de
(1) Fraunhofer-Institute for Algorithms and Scientific Computing (SCAI), Schloss Birlinghoven, D-53754 Sankt Augustin, Germany
(2) 1st Department of Medicine, Christian-Albrechts-University Kiel, Schittenhelmstrasse 12, D -24105 Kiel, Germany
(3) Max-Planck-Institute for Informatics, Stuhlsatzenhausweg 85, D-66123 Saarbrücken, Germany

Inflammatory bowel disease comes in two forms: Crohn's disease and ulcerative colitis. Both of them are genetically complex, but are also influenced by environmental factors and have increasing prevalence and incidence. The two forms of the disease are of high interest, because until now very few is known about their aetiology. After the finding of NOD2 as an important gene for developing Crohn's disease, we analysed expression data of 33 persons and 35000 clones. Normalization and comparison of the expression levels of three groups of persons with different disease status (normal, Crohn's disease, and ulerative colitis) were conducted. We present new candidate genes and give some functional explanation of their influence to the disease.
[1]  Hampe, J., et al., Association between insertion mutation in NOD2 gene and Crohn's disease in German and British populations. Lancet, 2001. 357(9272): p. 1925-8.
[2] Hugot, J.P., et al., Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn's disease. Nature, 2001. 411(6837): p. 599-603.
[3] Cho, J.H., The Nod2 gene in Crohn's disease: implications for future research into the genetics and immunology of Crohn's disease. Inflamm Bowel Dis, 2001. 7(3): p. 271-5.
[4] Van Heel, D.A., et al., Inflammatory bowel disease is associated with a TNF polymorphism that affects an interaction between the OCT1 and NF-kappaB transcription factors. Hum Mol Genet, 2002. 11(11): p. 1281-9.
[5] Costello, C.M., Lu. T., Hampe, J., Eickhoff, H., Fölsch, U. R., Lehrach, H,, S. Schreiber, and N. 2038., Oral presentation at the 9th United European Gastroenterology Week, Amsterdam (2001): Expression screening analysis of mucosal samples from normals and patients with inflammatory bowel disease. Gut, 2001. 49(Suppl. III).
[6] Costello, C.M., et al., Oral presentation at the 2001 American Gastroenterological Association, San Diego, USA: Gene expression profiling in normal, Ulcerative Colitis (UC) and Crohn's Disease (CD) samples using high density cDNA arrays. Gastroenterology, 2000. 118(No 4(2)) (Suppl. III), No. 5171.
[7] Zien, A., et al., Centralization: a new method for the normalization of gene expression data. Bioinformatics, 2001. 17(Suppl 1): p. S323-31.
[8] Wilcoxon, F., Individual comparisons by ranking methods. Biometrics 1945. 1 : p. 80-83.
[9] Ek, M., et al., Inflammatory response: pathway across the blood-brain barrier. Nature, 2001. 410(6827): p. 430-1.
[10] Jankowski, J.A., et al., Alterations in classical cadherins associated with progression in ulcerative and Crohn's colitis. Lab Invest, 1998. 78(9): p. 1155-67.