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Deciphering cancer: Investigating cell death mechanisms

This webinar is brought to you by the Science/AAAS Custom Publishing Office

Deciphering cancer: Investigating cell death mechanisms

Recorded 15 November 2017


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

You can also view Part 1, Part 2, Part 3, and Part 4 of this series.

Speaker bios

Andreas Strasser, Ph.D.

Walter and Eliza Hall Institute of Medical Research
Melbourne, Australia

Dr. Strasser is joint head of the Molecular Genetics of Cancer Division at The Walter and Eliza Hall Institute of Medical Research (WEHI) in Melbourne, Australia. He completed his M.S. and Ph.D. at the Basel Institute for Immunology and University of Basel in Switzerland, before joining WEHI as a postdoctoral fellow in 1989. He studies programmed cell death and how defects in apoptosis cause cancer or autoimmune disease and impair the response of tumor cells to anticancer therapy. Dr. Strasser and colleagues were the first to discover that abnormalities in cell death can cause cancer and autoimmune disease, including the discovery that BCL-2 collaborates with the MYC oncogene in tumorigenesis. Their research has determined which prosurvival BCL-2 family members are essential for the sustained growth of which cancers. They also found that BCL-2 and death receptors regulate distinct pathways to apoptosis, and have studied how the individual and overlapping roles of these two apoptotic pathways function in the immune system. Dr. Strasser discovered BIM and BMF, and was the first to show that BH3-only proteins are essential for the initiation of programmed cell death and stress-induced apoptosis. A collaboration between WEHI (including the Strasser group), Genentech, and AbbVie led to development of the BCL-2 inhibitor venetoclax, approved for treatment of refractory chronic lymphocytic leukemia, while a similar collaboration with Servier yielded the first potent and selective inhibitor of cell-death inhibitor MCL-1, currently in clinical trials.

Anthony G. Letai, M.D., Ph.D.

Dana-Farber Cancer Institute
Boston, MA

Dr. Letai received his M.D. and Ph.D. (under the direction of Elaine Fuchs) at the University of Chicago. He completed his clinical training in internal medicine at Brigham and Women’s Hospital in Boston, followed by a fellowship in hematology and oncology at Dana-Farber Cancer Institute, also in Boston. He was introduced to apoptosis and BCL-2 family proteins as a postdoctoral researcher in the laboratory of the late Stanley Korsmeyer. In 2004, Dr. Letai became an independent investigator at Harvard Medical School and the Dana-Farber Cancer Institute, where he is now an associate professor in medicine. His laboratory studies how apoptosis can be evaded, particularly in cancer cells, and how this evasion may be detected and targeted. Key to these studies is a novel assay—BH3 profiling—that can detect the pathways being used by the cells to evade apoptosis and how close a cell is to the threshold of apoptosis, providing useful and clinically relevant information. He has also led efforts to translate BCL-2, BCL-XL, and MCL-1 inhibitors into the clinic for the treatment of a range of hematologic cancers, including chronic lymphocytic leukemia, acute myeloid leukemia, acute lymphoblastic leukemia, and blastic plasmacytoid dendritic cell neoplasm. His lab is currently testing whether BH3 profiling can be used as a predictive biomarker in clinical cancer therapy.

Sean Sanders, Ph.D.

Washington, DC

Dr. Sanders did his undergraduate training at the University of Cape Town, South Africa, and his Ph.D. at the University of Cambridge, UK, supported by the Wellcome Trust. Following postdoctoral training at the National Institutes of Health and Georgetown University, Dr. Sanders joined TranXenoGen, a startup biotechnology company in Massachusetts working on avian transgenics. Pursuing his parallel passion for writing and editing, Dr. Sanders joined BioTechniques as an editor, before joining Science/AAAS in 2006. Currently Dr. Sanders is the Senior Editor for Custom Publishing for the journal Science and Program Director for Outreach.

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