Autoimmune and Cardiovascular Diseases: Insight into Inflammatory Pathways
Principal Investigator: Robert M. Plenge, M.D., Ph.D., Divison of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital; Broad Institute of MIT and Harvard University
Co-Investigators: Katherine P. Liao, M.D., Elizabeth W. Karlson, M.D., Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital; Phillip De Jager, M.D., Ph.D., Zongqi Xia, M.D., Ph.D., Department of Neurology, Brigham and Women's Hospital; Ashwin Ananthakrishnan, M.D., Department of Gastroenterology, Massachusetts General Hospital.
What questions are we asking in this DBP?
Can we identify genes that influence risk of rheumatoid arthritis (RA), multiple sclerosis (MS) and inflammatory bowel disease (IBD)? Moreover, can we query electronic medical records for patient characteristics that predict pre-clinical manifestations (e.g., demyelinating disease on MRI for pre-MS), severe disease (e.g., fistulas for IBD), and treatment response (e.g., anti-TNF therapy for RA)? In particular, we will focus on coronary artery disease (CAD) in all three autoimmune diseases to search for immune-mediated mechanisms that underlie CAD.
How will i2b2 help us answer these questions?
The i2b2 team will provide the technical expertise to perform queries of electronic medical records, including NLP interrogation of written notes, to identify RA, MS and IBD patients and relevant clinical data.
What tools do we anticipate will be developed from our work that will be of value to others?
Our project will require novel tools for applying Natural Language Processing (NLP) text extraction utilities. Specifically, we will require tools to extract information on autoantibody status, radiographic changes, treatment with medications, and environmental exposures (e.g., smoking).
What new clinical discoveries do we anticipate may arise from our work?
We anticipate that we will find new genes that influence risk of RA, MS and IBD. In addition, we may find genes and serological factors (e.g., autoantibodies) that predispose to CAD.