Title

The Role of Spy1 During Mammary Involution

Standing

Undergraduate

Type of Proposal

Oral Research Presentation

Challenges Theme

Building Viable, Healthy and Safe Communities

Your Location

University of Windsor

Faculty

Faculty of Science

Faculty Sponsor

Dr. Lisa Porter

Abstract/Description of Original Work

One in eight women will be diagnosed with breast cancer in her lifetime. From puberty to menopause, risk of breast cancer fluctuates with the natural development of the breasts. A period of increased breast cancer risk, metastatic potential, and mortality occurs following childbirth. Recent preliminary research suggests the propensity of postpartum breast cancer (PPBC) is enabled by the natural process of involution: when the mammary gland reverts to non-lactating tissue by balancing high rates of cell death regeneration via stem cells. This death and regeneration are controlled by the cell cycle; a particular cell cycle regulator, the atypical protein Spy1, is capable of enabling cell proliferation, protecting stem cells, and overriding cell death. Spy1 levels have been found to be elevated in all forms of breast cancers. Interestingly, levels of Spy1 are similarly elevated during involution. We hypothesize that Spy1 protects the stem cell population necessary for normal mammary gland reconstitution post involution. This project aims to establish Spy1 manipulated involution models by mimicking pregnancy-lactation-involution hormonal cues in vitro and investigate how Spy1 affects mammary gland changes during involution in vivo to determine the effect of Spy1 on mammary stem cells during involution. Understanding Spy1-involution dynamics may reveal how its alterations may potentially lead to aggressive PPBC – beginning the characterisation of this unique subtype and highlighting Spy1 as a target for screening, diagnostic, and treatment. Increasing the scope of postpartum maternal care to include breast cancer perspectives is crucial for improving the care and outcome of PPBC patients.

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The Role of Spy1 During Mammary Involution

One in eight women will be diagnosed with breast cancer in her lifetime. From puberty to menopause, risk of breast cancer fluctuates with the natural development of the breasts. A period of increased breast cancer risk, metastatic potential, and mortality occurs following childbirth. Recent preliminary research suggests the propensity of postpartum breast cancer (PPBC) is enabled by the natural process of involution: when the mammary gland reverts to non-lactating tissue by balancing high rates of cell death regeneration via stem cells. This death and regeneration are controlled by the cell cycle; a particular cell cycle regulator, the atypical protein Spy1, is capable of enabling cell proliferation, protecting stem cells, and overriding cell death. Spy1 levels have been found to be elevated in all forms of breast cancers. Interestingly, levels of Spy1 are similarly elevated during involution. We hypothesize that Spy1 protects the stem cell population necessary for normal mammary gland reconstitution post involution. This project aims to establish Spy1 manipulated involution models by mimicking pregnancy-lactation-involution hormonal cues in vitro and investigate how Spy1 affects mammary gland changes during involution in vivo to determine the effect of Spy1 on mammary stem cells during involution. Understanding Spy1-involution dynamics may reveal how its alterations may potentially lead to aggressive PPBC – beginning the characterisation of this unique subtype and highlighting Spy1 as a target for screening, diagnostic, and treatment. Increasing the scope of postpartum maternal care to include breast cancer perspectives is crucial for improving the care and outcome of PPBC patients.