2008 – Present
I study how Spy1’s role in cell processes, such as invasion and migration, during normal mammary gland development and how it is involved in breast cancer progression and metastasis. I use an in vitro 3D cell culture model as well as an exciting new in vivo 3D zebrafish metastasis model, allowing us to study Spy1 in more biologically relevant systems.
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.
2014 – Present
My research is focused on the role of cell cycle regulation mechanisms in bypassing senescent barriers and implications this may have on cellular reprogramming, stem cells and tumourigenesis in the central nervous system. I study the role of Spy1 in these processes using in vitro colony formation and neurosphere assays as well as in vivo mouse model system.
Martin Khosravi Bakht
2016 – Present
My work primarily focuses on the identification of Spy1-related cell cycle mechanisms that are potentially involved in neuroendocrine prostate cancer and triple negative breast cancer. In addition, I am interested in the role of androgen receptor in progression, linage plasticity and radio/chemo-resistance of prostate and breast cancers. I study in vitro cell line models and in vivo animal models using a variety of cancer cell biology methods such as immunostaining, western blot and qPCR.
2017 – Present (Collaboration with Dr. Andrew Swan)
Tuberin is an important cell cycle regulator, primarily involved in nutrient sensing and the mTOR pathway. It has also been implicated in G2/M regulation, however this role has not been very well characterized. My project focuses on the role of Tuberin in regulating entry into mitosis, specific its role in regulating Cyclin B for mitotic entry. I use cell culture based methods to examine the Cyclin B-Tuberin interaction in human cells, and further, examine the nature of this interaction in the genetic model system Drosophila melanogaster (fruit flies). We hope to understand how cells enter mitosis, and how Tuberin regulates this important cell cycle transition both in humans, and in Drosophila.
2015 – Present
Resistance to treatment and disease recurrence remains a difficult hurdle in treating triple-negative breast cancers. Even though patient responses are positive to initial treatment, disease recurrence is still a major concern for 10-15% of patients. It is also speculated that cells that have the highest resistance to standard of care chemotherapy also possess stem-like qualities. In my research, I focus on alternative methods of identifying the stem-like population by use of reporter constructs for two important isoforms of ALDH1 that are important in maintaining stemness. Once further characterized, these constructs will also be used to identify the remaining population that are resistant to treatment both in vitro and in vivo models.
2016 – Present
My research is focused on determining the mechanistic effects of the novel cell cycle regulator Spy1 in mammary development. I am specifically interested in the changes to developmental pathways and phenotypic effects that could draw similarities to tumorigenesis. I use in-vitro cell culture to manipulate levels of Spy1 and its downstream targets as well as a in-vivo mouse model.
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.