Functional Genomics to Study Cancer
We are using genome-scale CRISPR-Cas9 genetic screens in a large number of human cancer cell lines to study cancer. With this approach we are defining oncogenic drivers, synthetic lethal interactions, and genes that modulate the response to drug therapies. I will discuss the big picture lessons we have learned as well as the challenges we have encountered. I will also present efforts to develop tissue culture media that better mimics the metabolic composition of human plasma and our efforts to understand how the metabolic milieu affects the genetic dependencies of cancer cells.
David Sabatini is a Member of the Whitehead Institute for Biomedical Research, and a Professor of Biology at the Massachusetts Institute of Technology. He is also an Investigator of the Howard Hughes Medical Institute, a Senior Associate Member at the Broad Institute and a member of the Koch Institute for Integrative Cancer Research.
David and his lab study the basic mechanisms that regulate cell growth. A major focus of the lab is the Target of Rapamycin (TOR) pathway, a major regulator of growth in many eukaryotic species. This has resulted in the identification of many components of the pathway and to an understanding of their cellular and organismal functions, most of which have implications for diseases such as cancer and diabetes. David is also interested in the role of metabolism in cancer and in the mechanisms that control the effects of dietary restriction on tumorigenesis. Additionally, his lab has developed new technologies that facilitate the analysis of gene function in mammalian cells.