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Grant: Project Grant

McMaster University

$837,675.00

Characterization of a novel prostate cancer factor contactin 1 (CNTN1)-derived tumorigenesis through establishing a new transgenic mouse model for prostate cancer

EF 2023-24

Résumé
Prostate cancer (PC) affects one in six men and is the second leading cause of cancer-associated deaths in Canadian men. Mortality is caused by cancer progression. A major progression is recurrence following initial therapy. Recurrent PCs have higher risks of metastasis. The standard treatment for metastatic PCs is androgen deprivation therapy (ADT). This treatment temporarily halts cancer growth; but resistant tumors as castration resistant prostate cancers (CRPCs) commonly arise. CRPCs remain lethal. Thus, the typical processes of PC mortality include tumor formation and progression to recurrent tumors, metastasis, and CRPC. To improve patient management, we need a better understanding of factors regulating these processes. We have recently discovered contactin 1 (CNTN1) as a new factor promoting prostate cancer. Examination of more than 600 prostate cancer samples directly obtained from patients demonstrated an association of CNTN1 with PC recurrence. In our research using mouse models for PC, CNTN1 was able to initiate PC, promote PC metastasis, and associate with CRPC progression. Our work thus revealed CNTN1 as a novel factor enhancing PC initiation, metastasis, and CRPC. In this research, we will thoroughly examine CNTN1's role in PC formation, progression and the mechanisms by which CNTN1 promotes PC. This investigation will produce new knowledge on a novel and critical prostate cancer factor (CNTN1), and may lead to novel therapeutic interventions to inhibit CNTN1 function in hopes of slowing PC formation and progression. This research is unique. CNTN1 is a newly discovered factor in promoting prostate cancer formation and progression. Importantly, we were the pioneers in discovering CNTN1 being a novel prostate cancer factor, which was published in a leading cancer research journal. We remain the leading group worldwide to investigate CNTN1-mediated prostate cancer formation and progression.
Programme
Project Grant
Bénéficiaire
Emplacement
Ontario, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database

Tel que publié

Id
488928
Name
Tang Damu
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Cancer Research
Theme2
Biomedical
Prcname2
Cancer Biology & Therapeutics 2
Projecttitle
Characterization of a novel prostate cancer factor contactin 1 (CNTN1)-derived tumorigenesis through establishing a new transgenic mouse model for prostate cancer
Programtype2
Operating Grants
Orgnameinp2
McMaster University
Cihramount2
$837,675
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Contactin 1 (Cntn1); Prostate Cancer; Transgenic Mouse Model For Prostate Cancer
Abstract
Prostate cancer (PC) affects one in six men and is the second leading cause of cancer-associated deaths in Canadian men. Mortality is caused by cancer progression. A major progression is recurrence following initial therapy. Recurrent PCs have higher risks of metastasis. The standard treatment for metastatic PCs is androgen deprivation therapy (ADT). This treatment temporarily halts cancer growth; but resistant tumors as castration resistant prostate cancers (CRPCs) commonly arise. CRPCs remain lethal. Thus, the typical processes of PC mortality include tumor formation and progression to recurrent tumors, metastasis, and CRPC. To improve patient management, we need a better understanding of factors regulating these processes. We have recently discovered contactin 1 (CNTN1) as a new factor promoting prostate cancer. Examination of more than 600 prostate cancer samples directly obtained from patients demonstrated an association of CNTN1 with PC recurrence. In our research using mouse models for PC, CNTN1 was able to initiate PC, promote PC metastasis, and associate with CRPC progression. Our work thus revealed CNTN1 as a novel factor enhancing PC initiation, metastasis, and CRPC. In this research, we will thoroughly examine CNTN1's role in PC formation, progression and the mechanisms by which CNTN1 promotes PC. This investigation will produce new knowledge on a novel and critical prostate cancer factor (CNTN1), and may lead to novel therapeutic interventions to inhibit CNTN1 function in hopes of slowing PC formation and progression. This research is unique. CNTN1 is a newly discovered factor in promoting prostate cancer formation and progression. Importantly, we were the pioneers in discovering CNTN1 being a novel prostate cancer factor, which was published in a leading cancer research journal. We remain the leading group worldwide to investigate CNTN1-mediated prostate cancer formation and progression.
Competitiondate
202309
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Tang, Damu
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $837,675~ $0~