Samuel Benchimol, Professor, Department of Biology, York University,

Canada Research Chair in Biomedical Health. 

Before joining York University in 2006, Dr Benchimol was a Senior Scientist at the Ontario Cancer Institute and Professor in the Department of Medical Biophysics, University of Toronto.  He served as Acting Chair of the Department of Medical Biophysics from 2000 to 2002 and as Head of the Division of Cell and Molecular Biology at the Ontario Cancer Institute from 1993 to 2005.  He has served on numerous committees for granting agencies in Canada and in the USA.  He served as a member of the editorial board of Oncogene from 1990 to 2000.  He is a member of the International Scientific Council for the Israel Cancer Research Fund and he serves on the Scientific Advisory Board of Eleos, Inc.

His research interests lie in understanding the mechanisms involved in cell growth regulation and in malignancy.  A large part of his work has focused on the p53 tumour suppressor gene with the aim of understanding how p53 regulates cell growth.  The p53 tumour suppressor gene is inactivated by mutation in about 50% of all human cancer.  The loss of p53 protein function is an important event in  the development of cancer.  His studies of Friend virus-induced murine erythroleukemia provided an early indication that p53 was a negative regulator of cell growth and that p53 could act as a tumour suppressor.

Dr. Benchimol is studying how the p53 protein functions to suppress tumour formation.  p53 protein is known to bind to DNA in a very specific manner and to promote the expression of p53-responsive genes.  In normal cells, p53 is expressed as an inactive protein. However, in response to various types of stress - for example, DNA damage and  inappropriate growth signals - p53 becomes activated and regulates the expression of a large number of genes, leading to cell death or inhibition of cell growth. Getting rid of these damaged cells and restricting cells that are growing inappropriately is beneficial because these cells often lead to cancer.

His group recently identified two novel genes that are transcriptionally regulated by p53.  One encodes a pro-apoptotic protein called Pidd that is induced by DNA damage in a p53-dependent manner and is required for p53-dependent apoptosis.  The other called Pirh2 encodes an E3 ubiquitin ligase that binds p53 protein and promotes its degradation.  Related work in his laboratory centres on understanding how extracellular survival signals and intracellular factors affect the cellular response to p53 activation and to other stress stimuli.   He is also interested in the involvement of p53 and telomerase in controlling the replicative lifespan of human cells.  His group showed that overexpression of the telomerase catalytic subunit was sufficient for telomere elongation and for extension of cellular lifespan providing evidence that telomere shortening in human cells signals cells to enter senescence. His group also showed that p53 protein becomes activated as cells age in culture.  The relationship between cellular aging, cancer and p53 is actively being studied using genomic and proteomic approaches.

Dr. Benchimol has more than ninety publications in top scientific journals including Blood, Cell, Current Biology, EMBO Journal, Genes and Development, Molecular Cell, Molecular and Cellular Biology, Nature, Nature Genetics and Proceedings of the National Academy of Sciences.