Academic Rank:
Professor, UBC

Short Bio:

Ed Conway was born and educated in Toronto, receiving degrees in Electrical Engineering and Medicine at the University of Toronto. He completed fellowships in Hematology-Oncology at Harvard University and MIT and returned to Toronto as a physician-scientist and hematologist. In 1995, Ed was recruited to the University of Leuven in Belgium, where he led a research group focused on vascular disease and inflammation, coordinated collaborations with industry, and organized graduate educational programs. Ed was repatriated back to Canada in 2009 as the Director of UBC’s Centre for Blood Research where his goal is to catalyze translational research between basic and clinical scientists and to promote the development of education and training programs for the next generation of medical scientist health professionals. His research is designed to characterize the molecular mechanisms underlying disease using a range of technologies, from bench to bedside. He is supported by grants from the Heart and Stroke Foundation, the CIHR, NSERC, MITACs, CanVECTOR, CFI and the CRC program.


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.