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Grant: Project Grant

University of Toronto

$1,025,100.00

Molecular characterization of RAS GTPase

FY 2018-19

Summary
RAS is one of the most frequently mutated cancer-causing genes that govern several cellular processes critical for cancer cell survival and growth. Despite intensive efforts since its discovery over three decades ago, drugs directed against RAS have ultimately failed in the clinic, in part due to our incomplete understanding of how RAS is regulated, prompting the widely held perception that RAS is 'undruggable'. Recently, we made a seminal discovery showing that RAS when phosphorylated (a type of modification) is effectively turned 'OFF', while when de-phosphorylated (removal of modification) RAS is turned 'ON'. Armed with this new knowledge, we showed that RAS could be inactivated indirectly by blocking its de-phosphorylation (i.e., activation) process. In this proposal, we will elucidate precisely how these modifications regulate the activity of RAS, which will significantly advance our molecular understanding of this commonly mutated gene in cancer with the supposition that lessons learned will also lay the foundation for the development of novel cancer therapies.
Program
Project Grant
Location
Ontario, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database

As published

Id
400827
Name
Ohh Michael
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Cancer Research
Theme2
Biomedical
Prcname2
Molecular & Cellular Biology of Cancer
Projecttitle
Molecular characterization of RAS GTPase
Programtype2
Operating Grants
Orgnameinp2
University of Toronto
Cihramount2
$1,025,100
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Phosphorylation; Ras; Signalling
Abstract
RAS is one of the most frequently mutated cancer-causing genes that govern several cellular processes critical for cancer cell survival and growth. Despite intensive efforts since its discovery over three decades ago, drugs directed against RAS have ultimately failed in the clinic, in part due to our incomplete understanding of how RAS is regulated, prompting the widely held perception that RAS is 'undruggable'. Recently, we made a seminal discovery showing that RAS when phosphorylated (a type of modification) is effectively turned 'OFF', while when de-phosphorylated (removal of modification) RAS is turned 'ON'. Armed with this new knowledge, we showed that RAS could be inactivated indirectly by blocking its de-phosphorylation (i.e., activation) process. In this proposal, we will elucidate precisely how these modifications regulate the activity of RAS, which will significantly advance our molecular understanding of this commonly mutated gene in cancer with the supposition that lessons learned will also lay the foundation for the development of novel cancer therapies.
Competitiondate
201903
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Ohh, Michael
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $1,025,100~ $0~
University of Toronto - $1,025,100 Grant (2018-19) | Canada Spends