Kris pursued graduate training in Molecular and Cellular Pharmacology at the University of Miami School of Medicine under the mentorship of Izidore Lossos, MD. After receiving his PhD, Kris joined the laboratory of Anthony Letai, MD, PhD, at the Dana-Farber Cancer Institute/ Harvard Medical School for his postdoctoral fellowship.
In collaboration with others in the Letai laboratory, Kris found that some patients with cancers including ovarian cancer have tumors that are more highly primed to undergo programmed cell death (apoptosis) than others, as measured by a novel assay called BH3 Profiling (Ni Chonghaile & Sarosiek, et al., Science, 2011). Cancer cells and patient tumors that are more primed to undergo apoptosis are consequently more sensitive to chemotherapy treatment. This finding potentially explains why some patients respond favorably to chemotherapy while others do not. Kris has also utilized BH3 profiling to identify novel interaction preferences among the BCL-2 family of proteins, finding that BID preferentially activates BAK while BIM preferentially activates BAX to trigger apoptosis (Sarosiek, et al., Molecular Cell, 2013)
More recently, Kris has characterized how apoptosis is regulated in healthy tissues and how this impacts cell fate decisions in response to damage and stress (Sarosiek, et al., Cancer Cell, 2017). A key finding of this work is that developmental regulation of apoptosis is a major determinant of the treatment-associated toxicities observed in adult and pediatric cancer patients. The Sarosiek Laboratory at Harvard School of Public Health in Boston is building on these findings by characterizing how cell death is regulated in healthy and diseased cells in order to expose novel opportunities for therapeutic intervention. Our multidisciplinary research team utilizes computational, genetic, biochemical, cellular and molecular approaches to study cell death regulation in vitro and in vivo. Current areas of focus include the modulation of cell death for ovarian cancer therapy and the elucidation of genetic and environmental mechanisms that alter apoptotic homeostasis to drive tumorigenesis.