Bruce William Stillman | |
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Born |
Melbourne, Australia |
16 October 1953
Residence | United States |
Fields | Biochemistry |
Institutions | Cold Spring Harbor Laboratory |
Alma mater |
University of Sydney (B.Sc. [Hons. 1]), Australian National University (PhD) |
Notable awards | Alfred P. Sloan, Jr. Prize,Louisa Gross Horwitz Prize |
Bruce William Stillman, AO, FAA, FRS (born 16 October 1953, in Melbourne, Australia) is a biochemist and cancer researcher who has served as the Director of Cold Spring Harbor Laboratory (CSHL) since 1994 and President since 2003. He also served as the Director of its NCI-designated Cancer Center for 25 years from 1992 to 2016. During his leadership, CSHL has been ranked as the No. 1 institution in molecular biology and genetics research by Thomson Reuters. Stillman’s research focuses on how chromosomes are duplicated in human cells and in yeast Saccharomyces cerevisiae; the mechanisms that ensure accurate inheritance of genetic material from one generation to the next; and how missteps in this process lead to cancer. For his accomplishments, Stillman has received numerous awards, including the Alfred P. Sloan, Jr. Prize in 2004 and the 2010 Louisa Gross Horwitz Prize, both of which he shared with Thomas J. Kelly of Memorial Sloan-Kettering Cancer Center.
Stillman was educated at Glen Waverley High School (1966-1969) and Sydney Boys High School (1970–71), then graduated with First Class honours from the University of Sydney, and earned his Ph.D. from the John Curtin School of Medical Research at the Australian National University.
He began his career at Cold Spring Harbor Laboratory in 1979 with investigations into how DNA is copied, starting with studying DNA replication of human adenovirus as a model. He then began to study how the genome of simian virus 40 (SV40) is duplicated in cells. Eventually his research focused on how cellular chromosomes are duplicated and how the entire process is regulated in cells, studying the process primarily in the yeast S. cerevisiae and in human cells. This work provided key insights into how both virus and cellular oncoproteins manipulate cellular physiology to bring about oncogenic transformation.