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Lee (Ted) A. Denson, MDAssociate Professor M. Susan Moyer Chair in Pediatric Inflammatory Bowel DiseaseDirector, Schubert-Martin Pediatric IBD CenterDepartment of Pediatrics; Division of Gastroenterology, Hepatology and NutritionVisit the Denson Lab Site
The overarching goal of Dr. Denson’s research program is to discover pathogenic mechanisms that regulate both growth and mucosal inflammation in children with Inflammatory Bowel Disease, and thereby inform the development of new diagnostics and therapeutics. He has directed studies which have dissected fundamental molecular mechanisms of inflammatory growth hormone resistance in transgenic mice and tissue culture systems, and has designed and completed translational patient-based projects which have confirmed the relevance of pre-clinical findings. More recently, his group has tested the role of cytokine auto-antibodies in disease pathogenesis in animal models and patient-based studies, and has begun to develop these as biomarkers for complicated disease course. To this end, he has been actively involved in ongoing multi-center gene discovery efforts, prospective inception cohorts, and investigator-initiated and industry-supported clinical trials of new therapeutics. Dr. Denson currently serves on the steering committee multi-center RISK study to define clinical, genetic, and immune predictors of aggressive disease behavior in a prospective inception cohort of 1100 children with Crohn’s Disease. He is the co-PI for the PROTECT study, a NIH-sponsored multi-center clinical trial which will identify determinants of steroid-free remission with standardized medical therapy in a prospective inception cohort of 400 children with newly diagnosed Ulcerative Colitis.
Dr. Denson has used the Gene and Protein Expression and Bioinformatics Cores in collaboration with Dr. Aronow to identify genomic signatures that predict response to treatment of inflammatory bowel disease. He also collaborates with Drs. Han, Hogan, and Steinbrecher on various molecular mechanisms of IBD. Anticipated Core use: Gene and Protein Expression, Integrative Morphology, and Bioinformatics Cores.
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GM-CSF Ab and Susceptibility to NSAID-induced ileitis. Gm-csf deficient (GMKO), card15-deficient (C15KO), or wild type (WT) control mice were treated with a neutralizing GM-CSF antibody or isotype control and were placed on regular chow or chow containing the NSAID piroxicam 2 weeks later. The effect on ileal histopathology was determined. Original magnification, x100; bar = 50 micron. Figure from Gastroenterology, 2009;136:1261-1271.
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