Grant: Operating Grant
University of Manitoba
$754,049.00
Characterizing and Targeting Diminished RNF20 Expression in Cancer
FY 2010-11
Summary
Cancer is a leading cause of death worldwide. The World Health Organization (WHO) estimated that in 2008, ~7.6 million deaths worldwide were attributed to cancer. In Canada, the number of cancer-related deaths in 2010 was estimated at ~76,200. Despite the wealth of cancer research conducted each year and the various drugs available to combat cancer, the WHO forecasts that cancer-related deaths will continue to increase and claim ~12 million lives in 2030. What's more, many of the current drugs used to treat cancer are linked to a variety of side effects stemming from the nonspecific nature of the drugs employed. Accordingly, new treatment approaches and new drug targets must be identified that will not only enhance the specificity and effectiveness of those treatments, but eliminate or minimize many of the current side effects.
Defects in specific genes cause genome instability which is a common step required to convert normal cells into cancer cells. This instability most often results in the abnormal chromosome numbers which is a hallmark frequently found in nearly all tumor types. We believe the presence of abnormal chromosome numbers is an effective way to distinguish cancerous from normal cells and therefore is an attractive therapeutic target. As a result, we believe that the instability, or the defective genes causing the instability, can be used as a homing beacon to selectively and specifically target and kill cancerous cells while leaving normal cells unaffected. Thus, our major goal is to identify and characterize genes that regulate genome stability, and use this information to identify new drug targets that can specifically kill cells with defects in those genes. Using state-of- the-art approaches, we seek to uncover new and highly selective drug targets. The result of this work will dramatically impact the future development of cancer therapies, by increasing the specificity of cancer treatment while minimizing the adverse side effects.
Department
Program
Operating Grant
Recipient
Location
Manitoba, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
224377
Name
McManus Kirk J
Region
Manitoba
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Cancer Research
Theme2
Biomedical
Prcname2
Genetics
Projecttitle
Characterizing and Targeting Diminished RNF20 Expression in Cancer
Programtype2
Operating Grants
Orgnameinp2
University of Manitoba
Cihramount2
$754,049
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Cancer Genetics; Chromosome Instability; Cross-Species Approaches; High-Content Analysis; Novel Therapeutic Targets; Post-Translational Histone Modifications; Reverse Genetics; Rnf20; Synthetic Lethality; Tumorigenic Models
Abstract
Cancer is a leading cause of death worldwide. The World Health Organization (WHO) estimated that in 2008, ~7.6 million deaths worldwide were attributed to cancer. In Canada, the number of cancer-related deaths in 2010 was estimated at ~76,200. Despite the wealth of cancer research conducted each year and the various drugs available to combat cancer, the WHO forecasts that cancer-related deaths will continue to increase and claim ~12 million lives in 2030. What's more, many of the current drugs used to treat cancer are linked to a variety of side effects stemming from the nonspecific nature of the drugs employed. Accordingly, new treatment approaches and new drug targets must be identified that will not only enhance the specificity and effectiveness of those treatments, but eliminate or minimize many of the current side effects.
Defects in specific genes cause genome instability which is a common step required to convert normal cells into cancer cells. This instability most often results in the abnormal chromosome numbers which is a hallmark frequently found in nearly all tumor types. We believe the presence of abnormal chromosome numbers is an effective way to distinguish cancerous from normal cells and therefore is an attractive therapeutic target. As a result, we believe that the instability, or the defective genes causing the instability, can be used as a homing beacon to selectively and specifically target and kill cancerous cells while leaving normal cells unaffected. Thus, our major goal is to identify and characterize genes that regulate genome stability, and use this information to identify new drug targets that can specifically kill cells with defects in those genes. Using state-of- the-art approaches, we seek to uncover new and highly selective drug targets. The result of this work will dramatically impact the future development of cancer therapies, by increasing the specificity of cancer treatment while minimizing the adverse side effects.
Competitiondate
201103
Approvedterm2
5 yrs 0 mth
Pinamesdelim
McManus, Kirk J
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $754,049~ $0~