Autophagy is a cellular response to starvation and stress where cells form vesicles called autophagosomes that capture cellular components including organelles, protein aggregates and cytoplasm, which then fuse with lysosomes and are degraded. This lysosome-mediated cellular self cannibalization through autophagy serves multiple purposes including sustaining cellular energy homeostasis during starvation through recycling of cellular components, and damage mitigation though the clearance of unfolded proteins and dysfunctional organelles. Defects in autophagy have been implicated in many diseases including neurodegeneration, ageing, liver disease, and importantly, cancer. Autophagy localizes to metabolically stressed tumor regions and supports tumor cell survival prompting interest in modulating autophagy for cancer therapy. Moreover, most cancer therapeutics activate autophagy in tumor cells but how this impacts response is only beginning to be understood. Finally, oncogene and tumor suppressor gene pathways regulate autophagy and efforts are currently underway to define autophagy status in tumors and to determine the consequence to prognosis and therapeutic response.
Symposium: Autophagy, Metabolic Stress and Therapeutic Response

Tumor suppression by autophagy and therapeutic implications; Eileen P. White. UMDNJ-The Cancer Institute of New Jersey, New Brunswick, NJ

Autophagy control by oncogene and tumor suppressor gene products; Guido Kroemer. Institut Gustave Roussy, Villejuif, France

Autophagy in the control of tumor cell death; Kevin M. Ryan. Beatson Institute for Cancer Research, Glasgow, United Kingdom

Autophagy, cancer, and cancer therapeutics: Facts and fiction; Beth Levine. UT Southwestern Medical Center, Dallas, TX,