Project 461405
Defining the role of CDK6 and DNA repair pathways in tumorigenesis and identify CDK4/6-dependent synthetic lethal vulnerabilities in triple negative breast cancer.
Defining the role of CDK6 and DNA repair pathways in tumorigenesis and identify CDK4/6-dependent synthetic lethal vulnerabilities in triple negative breast cancer.
Project Information
| Study Type: | Unclear |
| Research Theme: | Biomedical |
Institution & Funding
| Principal Investigator(s): | Lebrun, Jean-Jacques |
| Institution: | McGill University Health Centre |
| CIHR Institute: | Cancer Research |
| Program: | |
| Peer Review Committee: | Molecular & Cellular Biology of Cancer |
| Competition Year: | 2022 |
| Term: | 5 yrs 0 mth |
Abstract 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.
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