Grant: Operating Grant
University of British Columbia
$763,047.00
The Androgen Receptor Signaling in Prostate Cancers
EF 2013-14
Résumé
Androgens are hormones produced and secreted by the testes. They have been strongly implicated in prostate cancers. These hormones act by activating a protein inside the cell called the androgen receptor (AR). The AR controls the levels of specific genes in cancer cells and promotes tumor growth. Therefore, drugs inhibiting AR function are used to treat patients with prostate cancers in advanced stages.
Unfortunately, this therapy is only effective for a short period of time. Though it is not clear why anti-AR therapies fail, recent research finds that cancer cells can produce a smaller form of AR, called AR-V7. AR-V7 stimulates tumor growth even under current anti-AR therapies. We therefore propose to investigate: 1) how the AR-V7 is generated; 2) whether the amount of AR-V7 protein in prostate tumors predicts the outcome of cancer patients; and 3) whether inhibition of AR-V7 function can provide a new opportunity for patients who fail anti-AR therapy.
Programme
Operating Grant
Bénéficiaire
Emplacement
British Columbia, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
307126
Name
Dong Xuesen
Region
British Columbia
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Cancer Research
Theme2
Clinical
Prcname2
Endocrinology
Projecttitle
The Androgen Receptor Signaling in Prostate Cancers
Programtype2
Operating Grants
Orgnameinp2
University of British Columbia
Cihramount2
$763,047
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Castration Resistant Prostate Cancer; Prostate Cancer
Abstract
Androgens are hormones produced and secreted by the testes. They have been strongly implicated in prostate cancers. These hormones act by activating a protein inside the cell called the androgen receptor (AR). The AR controls the levels of specific genes in cancer cells and promotes tumor growth. Therefore, drugs inhibiting AR function are used to treat patients with prostate cancers in advanced stages.
Unfortunately, this therapy is only effective for a short period of time. Though it is not clear why anti-AR therapies fail, recent research finds that cancer cells can produce a smaller form of AR, called AR-V7. AR-V7 stimulates tumor growth even under current anti-AR therapies. We therefore propose to investigate: 1) how the AR-V7 is generated; 2) whether the amount of AR-V7 protein in prostate tumors predicts the outcome of cancer patients; and 3) whether inhibition of AR-V7 function can provide a new opportunity for patients who fail anti-AR therapy.
Competitiondate
201403
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Dong, Xuesen
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $763,047~ $0~