The Lunenfeld-Tanenbaum Research Institute
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Dr. Daniel Durocher
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Dr. Daniel Durocher

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Lunenfeld-Tanenbaum
Research Institute
Mount Sinai Hospital
Joseph & Wolf Lebovic Health Complex
600 University Avenue
Toronto Ontario M5G 1X5

Tel: 416-586-4800 ext.2544
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Dr. Daniel Durocher   
SENIOR INVESTIGATOR

Dr. Daniel Durocher has focused his considerable talent on investigating how normal cells become cancer cells. His research is an example of the potential that drives fundamental research: that a new understanding of the basic cellular mechanisms involved in cancer, in all cancers, will revolutionize prevention and treatment of the disease.

In particular, Dr. Durocher is looking at how healthy cells detect and repair damage to their DNA. DNA damage to cells can occur through environmental exposure to sunlight or smoking, but also occurs regularly through normal metabolic processes like aging. We know that in healthy cells, this damage is detected and repaired naturally, but that in cancer this DNA damage response has failed.

Understanding how healthy cells detect and repair damage to their DNA will reveal important insights into what goes wrong in cells that become cancerous. Moreover, discoveries related to DNA damage will open the door to new, more sophisticated treatments for the disease: rendering cancer cells more vulnerable to chemotherapy for example, or developing drugs that can more selectively target cancerous cells.


Recently, Dr. Durocher and his team of researchers at the Lunenfeld-Tanenbaum discovered the function of a protein that is vital to the efficient repair of DNA damage.  This protein, called 53BP1, responds to a unique ‘flare’ signal called ubiquitin (another protein involved in cellular regulation), when there is DNA damage present and then works together to accelerate the repair process. 53BP1 protects the integrity of DNA by detecting two distinct marks at the site of DNA damage in the cell, and then helps direct repair of the damage, resulting in the re-joining of the broken DNA strands. When the DNA repair system is not functioning optimally in cells, mutations can go undetected and accumulate, potentially leading to abnormal growth and, eventually, tumours.

 

 

 

 

At a Glance

  • Investigates how normal cells become cancerous cells and how healthy cells detect and repair damage to their DNA. (In cancer, this DNA damage response has failed.)
  • Also studies telomeres the ends of chromosomes that are broken. There is a connection between aging and shortening telomeres.
  • Dr. Durocher is the Tom Kierans Research Chair in Mechanisms of Cancer Development.
  • Holds the Canada Research Chair in Proteomics, Bioinformatics and Functional Genomics.
  • Awarded the prestigious Maud Menten New Principal Investigator Prize from the Canadian Institutes of Health Research (CIHR) in 2006, and an Early Researcher Award from the Ontario Ministry of Research and Innovation in 2007
  • Winner of the 2009 Lloyd Fogler Award of Excellence
  • Named one of Canada's Top 40 Under 40 in 2010 

 

Major Research Activities

The major goal of Dr. Durocher´s lab is to understand how normal cells can become cancerous. Since genome instability is a hallmark of the cancer phenotype, his lab is studying DNA repair, DNA replication and cell cycle checkpoints, the gate keepers of the genome. Recently, Dr. Durocher took advantage of an exciting initiative in functional genomics to discover novel genes that enforce genome integrity.

 

Recent Publications

 

Document Actions
Ontario Health Study Faculty of Medicine, University of Toronto. mitacs honorary partner

 

 
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