2013 – Present
I am a Ph.D. student with interests in cancer and stem cell biology that include assessing diseased tissues and models of disease using modern microscopic techniques such as multicolour immunofluorescence and tissue microarrays.
2017 – Present
My research project focuses on the protein tuberin, which is a protein in the mTOR pathway that when mutated causes tuberous sclerosis. Specifically, I am interested in the binding pattern between tuberin and the mitotic cyclin, cyclin B1, and their interaction to act as a novel cell-cycle check at the G2/M phase. In addition, I am exploring the effects of the interaction between tuberin and the ERK pathway to better understand its role in tuberous sclerosis. I currently use in vitro methods and fly models to explore both of these aspects of tuberin interactions.
2018 – Present
Tuberin is a tumour suppressor that regulates the G1/S and G2/M phase of the cell cycle. My research project focuses on Tuberin’s interaction with the G2/M cyclin, Cyclin B1, and whether this leads to increased stability of the Tuberin protein. In addition, I am interested in whether this interaction aids in DNA damage repair through cell cycle arrest at the G2/M checkpoint. These will be addressed through in vitro methods, immunofluorescence, and flow cytometry. Dissecting this interaction will help our understanding of cell cycle regulation and importantly provide clues to the mechanisms of the tumour disorder, Tuberous Sclerosis.
M. Sc Candidate
Collaboration with Trant Lab (Department of Chemistry and Biochemistry)
2019 – Present
Samaneh Mehri is a graduate student at the University of Windsor under the supervision of Dr.Lisa Porter & Dr. John Trant. She joined the biomedical research group working on the development of therapies for cancer and autoimmune disease in fall 2019. Her research focuses on funded research into developing a treatment for autoimmune diseases.
2020 – Present
Recipient of 2020 NSERC Graduate Scholarship for Masters Program (CGS-M)
Young women face more aggressive breast cancers, entailing increased metastasis, increased disease recurrence, and decreased survival; suggesting that breast cancers in young women have uncharacterized unique biology. Parity has emerged as a variable in breast cancers in young women, potentially due to involution: the biological event in which the mammary gland reverts to non-lactating tissue. I study the role of Spy1 in normal mammary development particularly during this period of involution and how it may be implicated in tumorigenesis.
2020 – Present
Recipient of 2020 CIHR Graduate Scholarship for Masters Program (CGS-M)
My project focuses on Triple Negative Breast Cancer (TNBC). A rare subtype that occurs in 10-15% of diagnoses and tends to affect those of younger age or African American and Hispanic descent. Of importance, this subtype has a greater proportion of cells known as breast cancer stem cells (BCSC) compared to other subtypes. These are known to be resistant in the face of conventional therapy methods. My project will focus on investigating the cell cycle dynamics of the stem cell population following treatment with various drug combinations.
2020 – Present
Triple-negative breast cancer (TNBC) lacks three receptors (estrogen receptor, progesterone receptor, and HER2) that are commonly used as targets in breast cancer. Due to this, generalized chemotherapy treatments must be used to treat TNBC instead. One such treatment is ACT, an adjuvant chemotherapy. My project looks into how the efficacy of ACT (+Ca) is influenced by the administrative timing of each drug treatment and how SPY1 influences cell response to said drug treatments.
2020 – Present
Glioblastoma multiforme (GBM) is an aggressive type of brain cancer with median survival averaging 15 months post-diagnosis. Elevated levels of SPY1 in GBM are associated with the expansion of immature, drug-resistant, brain tumour initiating cell (BTIC) populations. Using in vitro and in vivo methods, my project explores how these elevated levels of SPY1 increase tumour aggressiveness during the initiation and/or progression of GBM through cooperation with selected mutations known to be associated with gliomas.