Cell death, including autophagy, necroptosis, and apoptosis, is a physiological process critical for normal development and function of multicellular organisms. Many of the signals that elicit cell death converge on mitochondria, which regulate cell death by a pivotal process called mitochondrial outer membrane permeabilization (MOMP). In apoptosis, MOMP is tightly regulated by the Bcl-2 family of proteins, composed of both proapoptotic (Bax, Bak, Bid, Bim) and antiapoptotic (Bcl-2, Bcl-xL, Bcl-W) members, which act in part by governing mitochondrial death signaling through cytochrome C release and subsequent activation of caspases. Irrespective of caspase activity, MOMP can lead to cell death by causing a progressive decline in mitochondrial function. Under certain circumstances, however, a cell can survive cell death; its survival may have pathophysiological consequences leading to cancer, autoimmunity, neurodegeneration, and resistance to cancer therapies. This webinar will examine how identification of dysregulated cell-death mechanisms underpinning various pathologies can be exploited to develop novel treatments for cancer and neurodegenerative diseases that directly activate the cell-death machinery.
During the webinar, viewers will learn about:
- Control pathways for various forms of cell death and their role in tumor development and response to anticancer therapeutics
- Which prosurvival Bcl-2 family members are essential for sustained survival and expansion of which cancers
- Using profiling assays to determine Bcl-2 family member arrangement on mitochondria and thereby to predict treatment response
- New methods to measure death signaling in mitochondria that provide clues to how an individual’s tumor cells will respond to therapy.
Questions can be submitted to the panel during the live broadcast.
This webinar will last for approximately 60 minutes