Ed Conway

Contact InformationEdC_29Aug2014
UBC Centre for Blood Research, Director
Life Sciences Centre
#4409 – 2350 Health Sciences Mall
Vancouver, BC, Canada V6T 1Z3
Tel: 1-604-822-4252
Fax: 1-604-822-7742
Cell: 1-778-960-7617
Email: ed.conway@ubc.ca

Current Positions

  • Professor of Medicine, University of British Columbia.
  • Canada Research Chair in Endothelial Cell Biology.
  • CSL-Behring Research Chair.
  • Staff Physician, Division of Hematology, Department of Medicine, VCH.
  • Adjunct Scientist, Canadian Blood Services.
  • Member – Experimental Medicine, Pathology and Laboratory Medicine.

Research Interests

Defining the molecular links between coagulation and innate immunity

Throughout evolution, organisms have developed means to simultaneously contain wounds by limiting bleeding with clot formation and fighting pathogens, thereby enabling rapid healing. Disease emerges when there is unchecked activation of the innate immune and/or coagulation responses. Indeed, simultaneous excess coagulation and innate immune responses are evident in numerous diseases, including, for example, atherosclerosis, stroke, coronary heart disease and diabetes, as well as organ ischemia-reperfusion, the metabolic syndrome, and other vasculopathic disorders, such as age-related macular degeneration, and hemolytic-uremic syndrome.

With the discovery that common molecular mechanisms regulate coagulation and inflammation, the last decades have seen major progress in identifying the cellular and molecular links. However, there remain major gaps in our knowledge and new discoveries are urgently needed for the development of novel strategies to prevent and/or treat cardiovascular disease and stroke. In our lab, we characterize the interplay between coagulation and complement, seeking relevant applications to our discoveries, using pre-clinical and clinical modeling approaches.

The perplexing story of the “tumor endothelial marker”, endosialin (CD248)

Endosialin (CD248) was originally identified as a tumor endothelial marker, but is now recognized to be expressed on the surface of activated stromal cells. This multi-domain glycoprotein is only expressed under pathologic conditions. Mice that lack CD248 are less sensitive to pro-inflammatory and oncogenic stimuli. We have determined that the cytoplasmic domain of CD248 modulates intracellular signals that promote tumor growth and inflammation. Ongoing studies are designed to identify molecular mechanisms by which CD248 functions, the protein partners with which CD248 interacts, and the wider impact of changes in expression of CD248. The findings may provide novel avenues for therapeutic targeting.

Selected Publications

https://www.ncbi.nlm.nih.gov/myncbi/14aXfz1e-lpkm/bibliography/public/

Education

  • Ph.D. (Biomedical Sciences), University of Leuven (KUL), Belgium, 2006.
  • M.B.A., Heriot Watt University, Scotland, 2004.
  • FACP, Harvard University, Boston, 1984.
  • FRCP(C), University of Toronto, 1984.
  • M.D., University of Toronto, 1979.
  • B.A.Sc. (Electrical Engineering), University of Toronto, 1975.