Relevant Degree Programs
Affiliations to Research Centres, Institutes & Clusters
Complete these steps before you reach out to a faculty member!
- Familiarize yourself with program requirements. You want to learn as much as possible from the information available to you before you reach out to a faculty member. Be sure to visit the graduate degree program listing and program-specific websites.
- Check whether the program requires you to seek commitment from a supervisor prior to submitting an application. For some programs this is an essential step while others match successful applicants with faculty members within the first year of study. This is either indicated in the program profile under "Admission Information & Requirements" - "Prepare Application" - "Supervision" or on the program website.
- Identify specific faculty members who are conducting research in your specific area of interest.
- Establish that your research interests align with the faculty member’s research interests.
- Read up on the faculty members in the program and the research being conducted in the department.
- Familiarize yourself with their work, read their recent publications and past theses/dissertations that they supervised. Be certain that their research is indeed what you are hoping to study.
- Compose an error-free and grammatically correct email addressed to your specifically targeted faculty member, and remember to use their correct titles.
- Do not send non-specific, mass emails to everyone in the department hoping for a match.
- Address the faculty members by name. Your contact should be genuine rather than generic.
- Include a brief outline of your academic background, why you are interested in working with the faculty member, and what experience you could bring to the department. The supervision enquiry form guides you with targeted questions. Ensure to craft compelling answers to these questions.
- Highlight your achievements and why you are a top student. Faculty members receive dozens of requests from prospective students and you may have less than 30 seconds to pique someone’s interest.
- Demonstrate that you are familiar with their research:
- Convey the specific ways you are a good fit for the program.
- Convey the specific ways the program/lab/faculty member is a good fit for the research you are interested in/already conducting.
- Be enthusiastic, but don’t overdo it.
G+PS regularly provides virtual sessions that focus on admission requirements and procedures and tips how to improve your application.
Graduate Student Supervision
Doctoral Student Supervision (Jan 2008 - Nov 2019)
Cell division requires the assembly and organization of a microtubule-based mitotic spindle. Microtubule assembly at multiple sites is dependent on Aurora kinase A activity, which is promoted through a complex with TPX2 (targeting protein for XKlp2). Subsequent organization of these microtubules and progression into anaphase requires balance between forces orchestrated by antagonistic motor complexes. My studies show that the non-motor protein RHAMM (receptor for hyaluronan mediated motility) integrates structural and biochemical pathways to ensure the fidelity of cell division. Silencing RHAMM in HeLa cells delayed the kinetics of spindle assembly. I located RHAMM to centrosomes and non-centrosome sites for microtubule nucleation and found it necessary for TPX2 localization and Aurora A activity at kinetochores. The RHAMM-TPX2 complex requires a conserved leucine zipper motif in RHAMM and a domain that includes the nuclear localization signal in TPX2. These findings indicate RHAMM is needed for spatially-regulated activation of Aurora A by TPX2, which coordinates spindle assembly. I monitored mouse embryonic fibroblasts deficient for RHAMM through division and identified defects progressing through the spindle checkpoint. In RHAMM-silenced HeLa cells, I identified sustained activation of the checkpoint with unfocused spindles and unattached kinetochores, implicating unbalanced motor activities mediated by kinesins. In metaphase-delayed cells, the abundance or location of checkpoint proteins was not altered. Moreover, aberrant spindle orientation could not account for each delayed division. In RHAMM-silenced cells, I found that the reciprocal immunoprecipitation of Eg5-TPX2, an inhibitory complex, was reduced and that the concurrent inhibition of Eg5-generated force recovered division kinetics. I also observed a prolonged metaphase delay in a proportion of RHAMM-silenced cells, which resolved through cohesion fatigue. Together, my findings indicate that RHAMM-mediated attenuation of Eg5-dependent outward forces is needed to align chromosomes and progress through division. Lastly, I identified defects in spindle structure and function in redundant models for RHAMM over-expression. Collectively, my studies demonstrate that RHAMM coordinates Aurora A signaling and balances motor forces that are needed for cell division. These findings provide novel insights into processes that are essential for mammalian cell division and the maintenance of genome stability.
Master's Student Supervision (2010 - 2018)
Malignant peripheral nerve sheath tumours (MPNST) are rare, hereditary cancers associated with neurofibromatosis type I. MPNSTs lack effective treatments as they often resist chemotherapies and have high rates of disease recurrence. Published analysis of copy number variation identified hemizygous loss of Hyaluronan Mediated Motility Receptor (HMMR, encodes RHAMM) in half of the examined high-grade MPNST, but not in benign neurofibromas or low grade tumours. RHAMM is a molecular brake for the mitotic kinase Aurora A (AURKA), so this loss of HMMR in high-grade MPNST may cause tumours to rely on AURKA activity and sensitizes them to aurora kinase inhibitors (AKI).Three MPNST cell-lines were profiled for the expression and activity of AURKA, as well as their responses to three AKI. The sensitivity of cell-lines with amplification of AURKA was reliant upon kinase activity, which correlated with the expression of the regulatory gene products TPX2 and RHAMM. Silencing of RHAMM, but not TPX2, increased AURKA activity and sensitized MPNST cells to AKI. All three AKIs reduced kinase activity in a dose-dependent manner, and AKI treatment induced cellular responses such as apoptosis, endoreduplication and cellular senescence. Additionally, two primary human MPNSTs grown in vivo as xenotransplants were treated with the AURKA-specific inhibitor MLN8237. Treatment resulted in tumour cells exiting the cell cycle and undergoing endoreduplication, which cumulated in stabilized disease. The MPNST cell-line S462 has a population of tumorigenic stem-like cells that can be grown in sphere culture. AURKA activity was critical to the propagation and self-renewal of sphere-enriched MPNST stem-like cells. AKI treatment significantly reduced the formation of spheroids, attenuated the self-renewal of spheroid forming cells, and promoted their differentiation. Silencing of TPX2 decreased AURKA activity, while silencing of RHAMM was sufficient to endow MPNST cells with an ability to form and maintain sphere culture. Collectively, our data indicate that AURKA is a rationale therapeutic target for MPNST, and tumour cell responses to AKI, which include differentiation, are modulated by the abundance of RHAMM and TPX2.
- A Model of Differential Mammary Growth Initiation by Stat3 and Asymmetric Integrin-α6 Inheritance. (2020)
- Hyaluronan Mediated Motility Receptor (HMMR) Encodes an Evolutionarily Conserved Homeostasis, Mitosis, and Meiosis Regulator Rather than a Hyaluronan Receptor (2020)
- FAM83D directs protein kinase CK1α to the mitotic spindle for proper spindle positioning. (2019)
- Genetic Instability (2019)
Encyclopedia of Cancer (3rd edition),
- CD44-mediated hyaluronan binding marks proliferating hematopoietic progenitor cells and promotes bone marrow engraftment. (2018)
- Hyaluronan-binding by CD44 reduces the memory potential of activated murine CD8 T cells. (2018)
European journal of immunology,
- The non-motor adaptor HMMR dampens Eg5-mediated forces to preserve the kinetics and integrity of chromosome segregation. (2018)
Molecular biology of the cell,
- Tumor Variant Identification That Accounts for the Unique Molecular Landscape of Pediatric Malignancies. (2018)
Jnci Cancer Spectrum,
- Anti-angiogenic treatment for breast cancer? (2017)
Cancer treatment reviews,
- BRCA1 controls the cell division axis and governs ploidy and phenotype in human mammary cells. (2017)
- Cell Cycle-Dependent Tumor Engraftment and Migration Are Enabled by Aurora-A. (2017)
Molecular cancer research : MCR,
- HMMR acts in the PLK1-dependent spindle positioning pathway and supports neural development. (2017)
- Assessing associations between the AURKA-HMMR-TPX2-TUBG1 functional module and breast cancer risk in BRCA1/2 mutation carriers. (2015)
- Designing a broad-spectrum integrative approach for cancer prevention and treatment. (2015)
Seminars in cancer biology,
- Genomic Instability and Cancer Metastasis (2015)
Cancer Metastasis - Biology and Treatment,
- Genomic instability in human cancer: Molecular insights and opportunities for therapeutic attack and prevention through diet and nutrition. (2015)
Seminars in cancer biology,
- Spatial regulation of Aurora A activity during mitotic spindle assembly requires RHAMM to correctly localize TPX2. (2014)
Cell cycle (Georgetown, Tex.),
- The Generation, Detection, and Prevention of Genomic Instability During Cancer Progression and Metastasis (2014)
Genomic Instability and Cancer Metastasis, , 15--38
- Tubers from patients with tuberous sclerosis complex are characterized by changes in microtubule biology through ROCK2 signalling. (2014)
The Journal of pathology,
- YB-1 transforms human mammary epithelial cells through chromatin remodeling leading to the development of basal-like breast cancer. (2014)
Stem cells (Dayton, Ohio),
- Genomic imbalance of HMMR/RHAMM regulates the sensitivity and response of malignant peripheral nerve sheath tumour cells to aurora kinase inhibition. (2013)
- The cytoskeletal protein RHAMM and ERK1/2 activity maintain the pluripotency of murine embryonic stem cells. (2013)
- Exploring the link between MORF4L1 and risk of breast cancer. (2011)
Breast cancer research : BCR,
- Interplay between BRCA1 and RHAMM regulates epithelial apicobasal polarization and may influence risk of breast cancer. (2011)
- YB-1 evokes susceptibility to cancer through cytokinesis failure, mitotic dysfunction and HER2 amplification. (2011)
- Multifunctional proteins bridge mitosis with motility and cancer with inflammation and arthritis. (2010)
- TACC3-TSC2 maintains nuclear envelope structure and controls cell division. (2010)
Cell cycle (Georgetown, Tex.),
- Targeting tumour-initiating cells to improve the cure rates for triple-negative breast cancer. (2010)
Expert reviews in molecular medicine,
- Biological convergence of cancer signatures. (2009)
- Aurora A kinase RNAi and small molecule inhibition of Aurora kinases with VE-465 induce apoptotic death in multiple myeloma cells. (2008)
Leukemia & lymphoma,
- Cell-surface and mitotic-spindle RHAMM: moonlighting or dual oncogenic functions? (2008)
Journal of cell science,
- Genetic and genomic analysis modeling of germline c-MYC overexpression and cancer susceptibility. (2008)
- Genetic interactions: the missing links for a better understanding of cancer susceptibility, progression and treatment. (2008)
- Targeted and nontargeted effects of ionizing radiation that impact genomic instability. (2008)
- Geometric approach to segmentation and protein localization in cell culture assays. (2007)
Journal of microscopy,
- Targeting aurora kinases as therapy in multiple myeloma. (2007)
- The selective Aurora B kinase inhibitor AZD1152 is a potential new treatment for multiple myeloma. (2007)
British journal of haematology,
- Intensity-based signal separation algorithm for accurate quantification of clustered centrosomes in tissue sections. (2006)
Microscopy research and technique,
- The pleiotropic roles of transforming growth factor beta in homeostasis and carcinogenesis of endocrine organs. (2006)
- A potential role for centrosomal deregulation within IgH translocation-positive myeloma. (2005)
- Hyaluronan and hyaluronan synthases: potential therapeutic targets in cancer. (2005)
Current drug targets. Cardiovascular & haematological disorders,
- Overexpression of transcripts originating from the MMSET locus characterizes all t(4;14)(p16;q32)-positive multiple myeloma patients. (2005)
- Receptor for hyaluronan-mediated motility correlates with centrosome abnormalities in multiple myeloma and maintains mitotic integrity. (2005)
- RHAMM expression and isoform balance predict aggressive disease and poor survival in multiple myeloma. (2004)
- Fluorescence imaging of multiple myeloma cells in a clinically relevant SCID/NOD in vivo model: biologic and clinical implications. (2003)
- RHAMM is a centrosomal protein that interacts with dynein and maintains spindle pole stability. (2003)
Molecular biology of the cell,
- In multiple myeloma, t(4;14)(p16;q32) is an adverse prognostic factor irrespective of FGFR3 expression. (2002)
- The integration of tissue structure and nuclear function. (2001)
Biochemistry and cell biology = Biochimie et biologie cellulaire,
- Lymphagenesis and cancer metastasis. (1998)
British journal of cancer,
Prospective Student Info Sessions
Faculty of Medicine Information SessionDate: Tuesday, 08 December 2020
Time: 11:00 to 12:00
UBC’s Faculty of Medicine is a global leader in both the science and the practice of medicine, and is home to more than 1,700 graduate students across over 20 graduate programs. In this session hosted by Dr Michael Hunt, Associate Dean, Graduate and Postdoctoral Education, we’ll provide an overview of the diverse array of graduate programs available, including cutting-edge research experiences in the biosciences, globally recognized population health education, quality health professional training, as well as certificate and online training options. Dr Hunt will also be joined by program advisors from across the faculty to take an inside look at the application process and provide some application tips to help make your application as strong as possible.