Grant: Project Grant
Research Institute of the McGill University Health Centre
$1,046,520.00
Defining the role of CDK6 and DNA repair pathways in tumorigenesis and identify CDK4/6-dependent synthetic lethal vulnerabilities in triple negative breast cancer.
FY 2021-22
Summary
Metastatic cancers are the most aggressive cancers, accounting for 90% of all cancer-related deaths. Radiation as well as chemotherapy are not effective enough to fight against these types of cancers. Our lab is studying triple-negative breast cancers (TNBCs), the most aggressive and the deadliest of all breast cancer molecular subtypes. Patients with TNBCs have limited treatment options and their life-threatening condition is most often clinically unfavorable. TNBC have poor prognosis, high metastasis rates, tumor recurrence and show resistance to conventional therapy. To date, there are no approved treatments or effective or approved targeted therapy against TNBC, highlighting a clear medical gap and unmet clinical need for these deadly tumors. The goal of this project is to develop an effective "targeted therapy" for these breast tumors. Our team has recently found that a protein called CDK6 could the DNA repair processes and lead to tumor progression in TNBC. We further found that blocking CDK6 and its downstream DNA repair target genes could efficiently block both the formation and the progression of TNBC tumors. Our objectives are to understand how CDK6 DNA repair functions affect cancer progression with the long-term goal of developing novel drugs that will help combat local and distant relapse and provide improved clinical benefits and outcome for TNBC patients.
Department
Program
Project Grant
Location
Quebec, Canada
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
461405
Name
Lebrun Jean-Jacques
Region
Québec
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Cancer Research
Theme2
Biomedical
Prcname2
Molecular & Cellular Biology of Cancer
Projecttitle
Defining the role of CDK6 and DNA repair pathways in tumorigenesis and identify CDK4/6-dependent synthetic lethal vulnerabilities in triple negative breast cancer.
Programtype2
Operating Grants
Orgnameinp2
Research Institute of the McGill University Health Centre
Cihramount2
$1,046,520
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Cdk4/6 Kinase Inhibitors; Combination Therapy; Crispr Genome-Wide Screen; Customized "Druggable Target" Crispr Library; Dna Repair; Nhej Inhibitors; Parp Inhibitors; Preclinical Models Of Breast Cancer; Synthetic Lethality; Triple Negative Breast Cancer
Abstract
Metastatic cancers are the most aggressive cancers, accounting for 90% of all cancer-related deaths. Radiation as well as chemotherapy are not effective enough to fight against these types of cancers. Our lab is studying triple-negative breast cancers (TNBCs), the most aggressive and the deadliest of all breast cancer molecular subtypes. Patients with TNBCs have limited treatment options and their life-threatening condition is most often clinically unfavorable. TNBC have poor prognosis, high metastasis rates, tumor recurrence and show resistance to conventional therapy. To date, there are no approved treatments or effective or approved targeted therapy against TNBC, highlighting a clear medical gap and unmet clinical need for these deadly tumors. The goal of this project is to develop an effective "targeted therapy" for these breast tumors. Our team has recently found that a protein called CDK6 could the DNA repair processes and lead to tumor progression in TNBC. We further found that blocking CDK6 and its downstream DNA repair target genes could efficiently block both the formation and the progression of TNBC tumors. Our objectives are to understand how CDK6 DNA repair functions affect cancer progression with the long-term goal of developing novel drugs that will help combat local and distant relapse and provide improved clinical benefits and outcome for TNBC patients.
Competitiondate
202203
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Lebrun, Jean-Jacques
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $1,046,520~ $0~