Standing
Undergraduate
Type of Proposal
Oral Research Presentation
Faculty
Faculty of Science
Faculty Sponsor
Lisa Porter
Proposal
The Role of Spy1 in Exacerbating the Long-Term Effects of Parity on the Mammary Gland
Khan, A.1, Fifield, B.1, Porter L.A.1.
1. University of Windsor, Windsor, Ontario. N9B 3P4.
Porter Lab, Department of Biomedical Sciences
Age is a significant variable in cancer development, and approximately 1/3 of breast cancer cases occur in patients older than 70. Another emerging risk factor is parity, or childbearing, which may be linked to cellular changes that affect a woman’s risk of developing breast cancer over the course of her lifetime. These changes are thought to result from the mammary gland not reverting to normal after lactation and involution - a developmental remodeling process where the milk secreting cells are cleared and replaced with adipocytes after weaning. Aberrant expression of the cyclin-like protein Spy1 has been shown to stimulate precocious development, resulting in disrupted morphology and oncogenesis within the mammary gland. Preliminary data suggests that the mammary glands of mice overexpressing Spy1 do not fully regress following lactation and involution, which may predispose them to breast cancer. We hypothesize that the overexpression of Spy1 exacerbates the long-term effects of parity on mammary gland morphology. To investigate this, we performed hematoxylin and eosin (H&E) staining as well as immunohistochemistry (IHC) on paraffin embedded sections, and whole mount staining of MMTV-Spy1 mice, a transgenic mouse model that overexpresses Spy1 within the mammary gland. We then compared the mammary gland morphology of parous MMTV-Spy1 mice to nulliparous MMTV-Spy1 mice, parous control FVB mice, and nulliparous control FVB mice. This research begins to improve our understanding of Spy1’s role in regulating proliferation and apoptosis, contributes to our overall knowledge of breast cancer dynamics, and further solidifies Spy1 as an important target for treatment.
Availability
Available March 29th (12-3 p.m), March 30th (12-2:30 p.m) March 31st (2-3 p.m), and April 1st (1-3 p.m)
Special Considerations
N/A
Spy1 and the Long-Term Effects of Childbearing on the Mammary Gland
The Role of Spy1 in Exacerbating the Long-Term Effects of Parity on the Mammary Gland
Khan, A.1, Fifield, B.1, Porter L.A.1.
1. University of Windsor, Windsor, Ontario. N9B 3P4.
Porter Lab, Department of Biomedical Sciences
Age is a significant variable in cancer development, and approximately 1/3 of breast cancer cases occur in patients older than 70. Another emerging risk factor is parity, or childbearing, which may be linked to cellular changes that affect a woman’s risk of developing breast cancer over the course of her lifetime. These changes are thought to result from the mammary gland not reverting to normal after lactation and involution - a developmental remodeling process where the milk secreting cells are cleared and replaced with adipocytes after weaning. Aberrant expression of the cyclin-like protein Spy1 has been shown to stimulate precocious development, resulting in disrupted morphology and oncogenesis within the mammary gland. Preliminary data suggests that the mammary glands of mice overexpressing Spy1 do not fully regress following lactation and involution, which may predispose them to breast cancer. We hypothesize that the overexpression of Spy1 exacerbates the long-term effects of parity on mammary gland morphology. To investigate this, we performed hematoxylin and eosin (H&E) staining as well as immunohistochemistry (IHC) on paraffin embedded sections, and whole mount staining of MMTV-Spy1 mice, a transgenic mouse model that overexpresses Spy1 within the mammary gland. We then compared the mammary gland morphology of parous MMTV-Spy1 mice to nulliparous MMTV-Spy1 mice, parous control FVB mice, and nulliparous control FVB mice. This research begins to improve our understanding of Spy1’s role in regulating proliferation and apoptosis, contributes to our overall knowledge of breast cancer dynamics, and further solidifies Spy1 as an important target for treatment.