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.