Dr Lewis Cantley will give the 2015 Milstein Lecture on Monday 14th December 2015 at 4.15pm in the LMB’s Max Perutz Lecture Theatre. The lecture, entitled “Phosphoinositide 3-Kinase and Cancer Metabolism” is open to anyone in the local area who is interested in attending.
Lewis is currently Director at the Meyer Cancer Center, Weill Cornell Medicine and New York Presbyterian Hospital, New York. His research is focused on understanding the biochemical pathways that regulate normal mammalian cell growth and the defects that cause cell transformation. His early work was on the structure and mechanism of enzymes that transport small molecules across cell membranes, and he pioneered the application of fluorescence resonance energy transfer (FRET) for studying such processes.
Lewis obtained a PhD in biophysical chemistry from Cornell University. He conducted postdoctoral research at Harvard University, where he was appointed assistant professor of biochemistry and molecular biology in 1978. He then became a professor of physiology in 1985 at Tufts University. Returning to Harvard Medical School in 1992 as professor of cell biology, he later become chief of Harvard’s new Division of Signal Transduction, and a founding member of its Department of Systems Biology. Lewis was appointed Director of the Beth Israel Deaconess Cancer Center in 2007. He then went on to join the faculty of Weill Cornell Medical College and New York-Presbyterian Hospital in 2012. Lewis is a fellow of the American Academy of Arts and Sciences and a member of the National Academy of Sciences.
Lecture abstract:
In general cancer cells produce higher levels of reactive oxygen species (ROS) than normal cells due to increased rates of metabolism and defective mitochondria. In order to survive under conditions of high ROS, cancer cells typically turn on pathways for generating NADPH and glutathione to bring ROS levels back to homeostasis. Activating mutations in PIK3CA or loss of PTEN or activating mutations in KRAS can stimulate glucose uptake and metabolism and pathways for generating NADPH and glutathione to suppress ROS. A detailed understanding of the biochemical mechanisms by which cancer cells suppress excess ROS may suggest new therapies for inducing synthetic lethality in tumors that evolve in specific mutational backgrounds. Our research using human cancer cell lines and genetically engineered mouse models suggests new approaches for killing cancer cells by targeting metabolic pathways for ROS suppression that allow cancer cells to survive.
Background information:
The Milstein Lecture, named in honour of the LMB Nobel Laureate César Milstein, is one of a series of lectures organised by the LMB and given by eminent scientists from around the world. César was born in Argentina in 1927. After completing PhDs in both Buenos Aires and Cambridge, and a brief spell of research back in Argentina, he joined the LMB in 1963 and spent the rest of his life here. He developed an early interest in immunology, and his research concentrated on antibody structure and diversity. In the early 1970′s he and his post-doc Georges Köhler developed the technique to produce monoclonal antibodies, for which they were jointly awarded the 1984 Nobel Prize in Physiology and Medicine. This technique has been used for diagnostics and developed further by LMB colleagues for therapeutic applications, leading to the creation of several MRC spin-out companies. César continued his research on how somatic mutation arises in immunoglobulin genes. He died in Cambridge on 24 March 2002.
