Michael Mowat

Biography

Biochemistry & Medical Genetics Graduate Affairs Committee, 2007-2013 Member, PhD Candidacy examination committees, 2005-09, 2011-13 Recruitment Committee-Assistant Professor 2010 Administrative Service - RIOH Associate Director (acting) 2011- 2012 Executive committee 2000-13 Chair, CancerCare MB library committee 1996-present Member, Space Committee 2000- present Member, Genomic Centre for Cancer Research and Diagnosis User Committee 2000-present

Research Interest

One area of research in my laboratory is the study of programmed cell death or apoptosis, a form of cell suicide. As a result of genetic changes, cancer cells have a reduced or slowed ability to undergo apoptosis, which can also make tumour cells more resistant to anti-cancer drug treatment. To better understand programmed cell death, we have taken a genetic approach. Several mutant cell lines have been isolated that are defective in apoptosis. This was done by using a specially constructed virus that, after it infects a cell, integrates into genes and interferes with their function. After selection for drug resistant cells, the underlying genes disrupted by the virus are studied for their role in programmed cell death and drug resistance. By understanding the genetic basis of resistance to cell death, completely new treatments can be devised. A gene that came out of these screens was the Dlc-2 (Deleted in liver cancer two) tumour suppressor gene. We are now studying the role this gene plays, along with the closely related Dlc-1 gene, in tumour cell progression and drug response. The Dlc-1 gene is found deleted in over 50 percent of breast, lung, liver and colon cancers. Also, the other normal copy of the gene is frequently silenced by promoter methylation. To study the role these genes play in the body, we have developed conditional knockout mouse models. With these mouse models, we can study the role the Dlc genes play in lung, and breast cancer spread through the body and anti-cancer drug response.