Standing
Undergraduate
Type of Proposal
Oral Research Presentation
Faculty
Faculty of Science
Faculty Sponsor
Lisa Porter
Proposal
Determining the Dependency of Spy1 based on Rb Status
Visconti, T., Philbin, N, Fifield, B, Porter L.A.
- University of Windsor, Windsor, Ontario. N9B 3P4
Porter Lab, Department of Integrative Biology/Biomedical Sciences
Breast cancer is the second most common cancer worldwide and the most common cancer among women. Triple Negative Breast Cancer (TNBC) is a particularly aggressive form of breast cancer with many subtypes based on gene expression profiles. There are currently no targeted treatments for TNBC due to its molecular characteristics, urging the discovery of new therapeutic targets. Potential therapeutic avenues are the cell cycle and its mediators which play an important role in cancer formation and progression. Spy1, a cyclin-like protein, promotes cell proliferation through the G1/S and G2/M checkpoints. Spy1 promotes proliferation even in the presence of DNA damage, overriding checkpoints and increasing cancer susceptibility. While Spy1 has been found to be elevated in breast cancer, its unique binding structure makes for an ideal candidate for cell cycle inhibition therapy. The retinoblastoma tumor suppressor protein (Rb) is known to regulate the DNA damage response system and is key in regulating the cell cycle. However, studies have shown that Rb is often mutated in TNBC inducing deregulated cell cycle progression potentially leading to tumor development. For some breast cancer subtypes the presence or absence of Rb (Rb status) can dictate response to treatment by cell cycle inhibitor drugs. Using in vitroTNBC models (MDA-MB-231 & Bt549 cell lines), this study aims to determine if Spy1 can override checkpoints independently of Rb status, and if elevated levels of Spy1 alter this response. These results could provide further guidance in developing cell cycle inhibition targeted therapies and potentially better TNBC patient outcomes.
Availability
March 29th, 30th from 12-1 and March 31st -April 1st from 12-3pm
Determining the Dependency of Spy1 based on Rb Status
Determining the Dependency of Spy1 based on Rb Status
Visconti, T., Philbin, N, Fifield, B, Porter L.A.
- University of Windsor, Windsor, Ontario. N9B 3P4
Porter Lab, Department of Integrative Biology/Biomedical Sciences
Breast cancer is the second most common cancer worldwide and the most common cancer among women. Triple Negative Breast Cancer (TNBC) is a particularly aggressive form of breast cancer with many subtypes based on gene expression profiles. There are currently no targeted treatments for TNBC due to its molecular characteristics, urging the discovery of new therapeutic targets. Potential therapeutic avenues are the cell cycle and its mediators which play an important role in cancer formation and progression. Spy1, a cyclin-like protein, promotes cell proliferation through the G1/S and G2/M checkpoints. Spy1 promotes proliferation even in the presence of DNA damage, overriding checkpoints and increasing cancer susceptibility. While Spy1 has been found to be elevated in breast cancer, its unique binding structure makes for an ideal candidate for cell cycle inhibition therapy. The retinoblastoma tumor suppressor protein (Rb) is known to regulate the DNA damage response system and is key in regulating the cell cycle. However, studies have shown that Rb is often mutated in TNBC inducing deregulated cell cycle progression potentially leading to tumor development. For some breast cancer subtypes the presence or absence of Rb (Rb status) can dictate response to treatment by cell cycle inhibitor drugs. Using in vitroTNBC models (MDA-MB-231 & Bt549 cell lines), this study aims to determine if Spy1 can override checkpoints independently of Rb status, and if elevated levels of Spy1 alter this response. These results could provide further guidance in developing cell cycle inhibition targeted therapies and potentially better TNBC patient outcomes.