This page contains a Flash digital edition of a book.
GENETIC MARKERS Discovering which genes are predictors of disease onset and severity.

Researcher Institution

Dr. Claude Asselin Université de Sherbrooke

Project How the cells lining the gut respond to microbes is Investment $119,445

controlled our genes. Dr. Asselin is studying the role (Year 3 of 3) of proteins, which control genetic and epigenetic information in gut cells during inflammation. In the long term, this research program will identify novel targets that could lead to better treatments for IBD.

Co-Investigator(s): Dr. Fernand

Keywords: intestinal epithelial cells; transcriptional regulation; autophagy; genetics; epigenetics.

Université de

Pierre-Gendron Sherbrooke Dr. Mark


Mount Sinai Hospital

Dr. Silverberg is evaluating the genes and microbes that are associated with the onset and recurrence

of inflammation following ileal resection for Crohn’s disease. This information will help healthcare professionals predict which Crohn’s disease patients are likely to develop recurrent inflammation after surgery.

Keywords: Crohn’

Dr. Thierrey Mallevaey

University of Toronto

s disease; disease recurrence; gene expression; mucosal inflammation; prognosis; surgery Mutations in genes encoding key bacteria-sensing . $119,445

molecules, called NOD1 and NOD2, are associated (Year 2 of 3) with the development of IBD. NOD proteins are believed to provide protective signals that prevent or dampen intestinal inflammation during the development of IBD, although their mechanisms of action are just beginning to be unraveled. Dr. Mallevaey is investigating whether NOD-mediated bacterial signals induce iNKT cell activation and afford them with protective functions during the development of IBD.

Keywords: natural killer T cells; innate immunity; lipid antigens; gene mutations.

Dr. Nicola Jones University of Toronto

Two gene mutations that are associated with Crohn’s disease are NOD2 (which senses bacteria


Dr. Dana Philpott University of Toronto

within the cell) and ATG16L1 (which is needed for digesting and recycling material inside the cell – called “autophagy”). In cells where NOD2 and ATG16L are not working properly this causes excessive inflammation. Dr. Jones will be studying how these two genes might be involved in causing disease in order to develop better therapies to treat and prevent IBD.

Keywords: autophagy; miRNA; NOD-like receptors; translational research; gene mutations.

15 | RESEARCH REPORT 2014 $119,445 (Year 3 of 4) $119,445 (Year 3 of 4)

Page 1  |  Page 2  |  Page 3  |  Page 4  |  Page 5  |  Page 6  |  Page 7  |  Page 8  |  Page 9  |  Page 10  |  Page 11  |  Page 12  |  Page 13  |  Page 14  |  Page 15  |  Page 16  |  Page 17  |  Page 18  |  Page 19  |  Page 20  |  Page 21  |  Page 22  |  Page 23  |  Page 24  |  Page 25  |  Page 26  |  Page 27  |  Page 28  |  Page 29  |  Page 30  |  Page 31  |  Page 32