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Grant: Project Grant

University of British Columbia

$1,028,925.00

Targeting CD47 in pediatric acute lymphoblastic leukemia.

EF 2020-21

Résumé
Cancer cells differ from normal ones in that changes adopted by cancer cells allow their continuous growth unchecked by processes that would limit it. A common adaptation is high level expression of CD47 as a pro-tumour antigen or marker, and that is linked to poor treatment outcomes and poor survivorship. As a convention, CD47 can be targeted therapeutically by blocking its function using inhibitory antibodies. We have discovered an antibody with the potential to not only block the CD47 antigen, but in fact directly trigger tumour cell death. We aim to understand how this process is triggered and to exploit this potential for effective anti-tumour responses for cancers that express high levels of CD47. Instead of CD47 functioning as a marker that supports tumour growth, we will engage its ability to effect self-suicide and develop this as a potential therapy for relapsed forms of childhood leukemia.
Programme
Project Grant
Emplacement
British Columbia, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database

Tel que publié

Id
433765
Name
Lim Chinten J
Region
British Columbia
Country
Canada
Orgtype
Research Institution; Institution Paid
Instname2
Cancer Research
Theme2
Biomedical
Prcname2
Molecular & Cellular Biology of Cancer
Projecttitle
Targeting CD47 in pediatric acute lymphoblastic leukemia.
Programtype2
Operating Grants
Orgnameinp2
University of British Columbia
Cihramount2
$1,028,925
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Cd47; Cell Death; Cell Survival; Chemotherapy; Leukemia; Macrophages; Oncogenic Drivers; Phagocytosis; Proteomics; Signal Transduction
Abstract
Cancer cells differ from normal ones in that changes adopted by cancer cells allow their continuous growth unchecked by processes that would limit it. A common adaptation is high level expression of CD47 as a pro-tumour antigen or marker, and that is linked to poor treatment outcomes and poor survivorship. As a convention, CD47 can be targeted therapeutically by blocking its function using inhibitory antibodies. We have discovered an antibody with the potential to not only block the CD47 antigen, but in fact directly trigger tumour cell death. We aim to understand how this process is triggered and to exploit this potential for effective anti-tumour responses for cancers that express high levels of CD47. Instead of CD47 functioning as a marker that supports tumour growth, we will engage its ability to effect self-suicide and develop this as a potential therapy for relapsed forms of childhood leukemia.
Competitiondate
202010
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Lim, Chinten J
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $1,028,925~ $0~