Costas A. Lyssiotis received his B.S. in Chemistry and Biochemistry from the University of Michigan in 2004. As a NSF Fellow, Costas earned a Ph.D. in the Schultz group at The Scripps Research Institute in 2010. There, his research focused on the identification and characterization of chemicals that reprogram cell fate. In particular, Costas and colleagues found that histone deacetylation is responsible for maintaining the lineage identity of oligodendrocyte precursor cells, where pharmacological inhibition of histone deacetylase activity reverts precursor cells back to the multipotent state. Subsequently, in collaboration with the Jaenisch lab at MIT, Costas and colleagues developed a small molecule screening platform that was used to identify chemical complements for the reprogramming factors that induce pluripotency in somatic cells. Implementation of this strategy led to the identification of compounds that replace the reprogramming factors Sox2 and Klf4. Current and future efforts with these compounds have begun to unravel the mechanisms at play during epigenome overhaul and may ultimately lead to the identification of a cocktail of small molecules that can convert somatic cells back to the pluripotent state.

Costas is currently pursuing post-doctoral studies in the Cantley lab at the Harvard Medical School as the Amgen fellow of the Damon Runyon Cancer Research Foundation. His research is focused on understanding the biochemical pathways and metabolic requirements of cancer cell proliferation and, in particular, how this information can be used to design targeted therapies | Curriculum Vitae