Philip Hieter

University of British Columbia


Election Year: 2016
Primary Section: 26, Genetics
Membership Type: Member

Biosketch

Philip Hieter is a Professor in the Michael Smith Laboratories at the University of British Columbia. He received his PhD in biochemistry from Johns Hopkins University in 1981, trained as a postdoctoral fellow at Stanford, and was a faculty member at the Johns Hopkins School of Medicine from 1985-1997. He moved to the University of British Columbia in 1997, and served as Director of the Michael Smith Laboratories until 2008. Dr. Hieter served as President of the Genetics Society of America in 2012. He is currently Chair of the CIHR Planning and Priorities Committee “Models and Mechanisms to Therapies”, and a Member of the Medical Advisory Board of the Gairdner Foundation. He is a Fellow of the Royal Society of Canada, Fellow of the Canadian Academy of Health Sciences, and Member of the American Academy of Arts and Sciences.

Dr Hieter is recognized for his work on structural and regulatory proteins that ensure faithful segregation of chromosomes during cell division, including seminal studies on yeast centromeres, sister chromatid cohesion, and regulation of cell cycle progression during mitosis. Throughout his career, his work has demonstrated and advocated the value of model experimental organisms for understanding mechanisms of human disease.

Research Interests

Dr Hieter is recognized for his work on structural and regulatory proteins that ensure faithful segregation of chromosomes during cell division. His work has also demonstrated and advocated the value of yeast and other model experimental organisms for understanding mechanisms of human disease. Over the past 30 years, his laboratory has developed and applied novel genetic, biochemical, and genomic methodologies to obtain a detailed understanding of the molecular components required for chromosome transmission in yeast, with the over-arching goal of relating his work in yeast to human cancer. Gene mutations causing a chromosome instability (CIN) phenotype in cancer cells represent a major predisposing condition in cancer initiation and/or progression. Current work in the Hieter laboratory includes a translational component, in which the extensive genome instability gene catalog that his laboratory has determined in yeast is being used to determine those genes that are somatically mutated and cause CIN in cancer. The Hieter laboratory then uses synthetic lethal genetic interaction data, based on yeast CIN genes whose human counterparts are mutated in cancers, to predict and validate novel drug targets for cancer therapy by a cross-species candidate approach.

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