Grant: Project Grant
University of Alberta
$818,550.00
Mechanisms and control of CD36-Fyn signal transduction by plasma membrane organization during anti-angiogenic response.
FY 2018-19
Summary
A critical step in cancer progression and expansion is the formation of novel blood supplies. This step known as the "angiogenic switch" corresponds to the formation, in the developing tumors, of novel blood vessels providing a source of nutrients, as well as a route for metastasis. This process is directly induced by cancer cells that concomitantly increase known activator (such as the Vascular endothelial growth factor (VEGF)) and decrease inhibitor (such as thrombospondin-1, TSP1) angiogenesis.
Several anti-angiogenic treatments are currently in use in the clinic and target primarily the EGF pathway. In the current project, we will investigate the mechanisms of TSP-1 inhibition of the angiogenic response with the goal to provide new alternative and complimentary treatments to many cancers.
This project will investigate TSP-1 signaling mechanisms via its receptor CD36 and its downstream effector Fyn.
Department
Program
Project Grant
Recipient
Location
Alberta, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
403506
Name
Touret Nicolas
Region
Alberta
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Genetics
Theme2
Biomedical
Prcname2
Cell and Developmental Physiology
Projecttitle
Mechanisms and control of CD36-Fyn signal transduction by plasma membrane organization during anti-angiogenic response.
Programtype2
Operating Grants
Orgnameinp2
University of Alberta
Cihramount2
$818,550
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Angiogenesis; Cd36; Lipid Nanodomains; Plasma Membrane Organization; Receptor Nanoclusters; Signal Transduction; Single Molecule Tracking; Src Family Kinase Fyn; Superresolution Microscopy
Abstract
A critical step in cancer progression and expansion is the formation of novel blood supplies. This step known as the "angiogenic switch" corresponds to the formation, in the developing tumors, of novel blood vessels providing a source of nutrients, as well as a route for metastasis. This process is directly induced by cancer cells that concomitantly increase known activator (such as the Vascular endothelial growth factor (VEGF)) and decrease inhibitor (such as thrombospondin-1, TSP1) angiogenesis.
Several anti-angiogenic treatments are currently in use in the clinic and target primarily the EGF pathway. In the current project, we will investigate the mechanisms of TSP-1 inhibition of the angiogenic response with the goal to provide new alternative and complimentary treatments to many cancers.
This project will investigate TSP-1 signaling mechanisms via its receptor CD36 and its downstream effector Fyn.
Competitiondate
201903
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Touret, Nicolas
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $818,550~ $0~
