Investigating the role of the non-canonical cyclin-like protein Spy1 in regulating the Breast Cancer Stem Cell population in Triple Negative Breast Cancer
Standing
Graduate (Masters)
Type of Proposal
Oral Research Presentation
Faculty
Faculty of Science
Faculty Sponsor
Dr. Lisa Porter, Dr. Bre-Anne Fifield
Proposal
Breast cancer is the most commonly diagnosed cancer in women, and treatment is often complicated by the tremendous heterogeneity of this disease. Triple Negative Breast Cancer (TNBC) occurs in 10-15% of diagnoses and typically has poorer outcomes than other subtypes of breast cancer. This is largely due to lack of targeted therapies and the existence of a greater proportion of cells known as breast cancer stem cells (BCSCs). BCSCs are more resistant to conventional therapy and are capable of driving patient relapse. The BCSC population characterized by a unique set of molecular markers and is further divided into subpopulations which have differential effects on the functional capabilities of the tumour and are associated with differing levels of clinical prognosis. Cell cycle mediators may play a key role in driving expansion of this population of dangerous cells. Spy1, a cyclin-like protein, promotes cell cycle progression through the G1/S, and the G2/M phases of the cell cycle and has been shown to be elevated in TNBC patients. Using an in vitro model of TNBC, the relative abundance of these BCSC subpopulations can be assessed to determine if increased levels of Spy1 can result in their expansion leading to more aggressive, invasive and fatal cancers. This work seeks to determine the differential effect of Spy1 on different BCSC subpopulations in hopes of elucidating future potential therapeutic promise.
Availability
March 29th 12-3pm, March 31st 12-3pm, April 1st 12-3pm
Investigating the role of the non-canonical cyclin-like protein Spy1 in regulating the Breast Cancer Stem Cell population in Triple Negative Breast Cancer
Breast cancer is the most commonly diagnosed cancer in women, and treatment is often complicated by the tremendous heterogeneity of this disease. Triple Negative Breast Cancer (TNBC) occurs in 10-15% of diagnoses and typically has poorer outcomes than other subtypes of breast cancer. This is largely due to lack of targeted therapies and the existence of a greater proportion of cells known as breast cancer stem cells (BCSCs). BCSCs are more resistant to conventional therapy and are capable of driving patient relapse. The BCSC population characterized by a unique set of molecular markers and is further divided into subpopulations which have differential effects on the functional capabilities of the tumour and are associated with differing levels of clinical prognosis. Cell cycle mediators may play a key role in driving expansion of this population of dangerous cells. Spy1, a cyclin-like protein, promotes cell cycle progression through the G1/S, and the G2/M phases of the cell cycle and has been shown to be elevated in TNBC patients. Using an in vitro model of TNBC, the relative abundance of these BCSC subpopulations can be assessed to determine if increased levels of Spy1 can result in their expansion leading to more aggressive, invasive and fatal cancers. This work seeks to determine the differential effect of Spy1 on different BCSC subpopulations in hopes of elucidating future potential therapeutic promise.