Title:
Assistant Professor

Institute:
Sunnybrook Health Sciences Centre, University of Toronto

Department:
Medical Oncology, Sunnybrook Odette Cancer Centre, Biological Sciences, Sunnybrook Research Institute

Province:
Ontario

Training:
Postdoctoral research fellow, Sunnybrook Research Institute, Toronto, Ontario, Canada
Clinical Research Fellow, Sunnybrook Odette Cancer Centre, Toronto, Ontario, Canada
MD, Medical School, University of Bern/Switzerland

Research interests:
Antivascular tumor therapy, therapeutic resistance, autophagy

Recognitions and awards:
Young Investigator Award 2011, Division of Medical Oncology, University of Toronto
Prostate Cancer Canada (PCC) Clinician-Scientist Award 2010-2012
Canadian Cancer Society Research Institute (CCSRI) Junior Investigator Grant Panel Travel Award 2010
Ontario Institute for Cancer Research (OICR) Clinician-Scientist II Investigator Award 2007-2010

Career highlights:
Characterization of differential resistance to metronomic versus conventional chemotherapy

Research Projects

Project title:
Studying autophagy as a complemetary therapeutic target in antivascular tumor therapy

Funding period: 
2011-2013

Program:
Operating Grant (Basic Research)

Summary:
Antivascular therapies impair tumor growth and prolong patient survival by reducing tumor blood flow. However, not all patients respond to this type of treatment, and most responders develop treatment resistance eventually. Tumor cell stress associated with antivascular therapy triggers autophagy, a cellular response that can enable either cell survival or cell death. Prolonged stress may result in autophagy-related tumor cell death, as suggested by recent studies of Dr. Emmenegger and his team analyzing resistance to antiangiogenic therapy, a form of chronic antivascular therapy. But the role of autophagy may be the opposite when applying so-called vascular disrupting agents, which result in acute, short-term cellular stress. To study these potentially dual effects of autophagy, tumors with distinct propensity to undergo autophagy grown in mice will be subjected to different antivascular therapies, followed by molecular analysis of various cell death mechanisms. The findings of these studies are expected to help optimizing the use of antivascular therapies.