Vincent Duronio


Relevant Degree Programs

Affiliations to Research Centres, Institutes & Clusters


Great Supervisor Week Mentions

Each year graduate students are encouraged to give kudos to their supervisors through social media and our website as part of #GreatSupervisorWeek. Below are students who mentioned this supervisor since the initiative was started in 2017.


Although, not directly as a supervisor, but as the program director, you've been a wonderful mentor to me! #GreatMentor Thank you Dr. Duronio for being encouraging, supportive, open-minded and thoughtful. As I approach the end of my doctoral journey, I am grateful for your support #Grateful

Michelle C (2019)


Graduate Student Supervision

Doctoral Student Supervision (Jan 2008 - May 2021)
Evaluation of the Role of ANGPTL4 in Tendon Vascularization (2016)

The mechanisms that regulate angiogenic activity in injured or mechanically loaded tendons are poorly understood. In this study we hypothesised that repetitive stretching of tendon cells alters the expression and release of angiogenic factors which may promote tendon vascularization. In order to examine the effects of repetitive stretching on the expression of angiogenic genes, primary human tendon cells were subjected to cyclic stretching. Cyclic stretching of two-dimensional primary tenocyte cell cultures increased the expression of VEGF, bFGF and Cox-2. But, by extending the time course, VEGF, bFGF and Cox-2 were progressively downregulated. Angiogenic profiling of tendon cells by qPCR array identified a number of other genes (ANGPTL4, FGF-1, TGFα, VEGF-C and SPHK1) that responded to tensile loading in a similar pattern. Further experiments revealed that cyclic stretching of human tendon fibroblasts stimulated the expression and release of ANGPTL4 protein via TGF-β and HIF-1α signalling. ANGPTL4 promoted the angiogenic activity of endothelial cells. Angiogenic activity was also increased following injury and following ANGPTL4 injection into mouse patellar tendons, whereas the patellar tendons of ANGPTL4 knock out mice displayed reduced angiogenesis following injury. In human rotator cuff tendons, there were both spatial and quantitative associations of ANGPTL4 with tendon endothelial cells. The experiments described in this thesis have shown that ANGPTL4 may assist in the regulation of vascularity in injured or mechanically loaded tendon. TGF-β and HIF-1α are two signalling pathways that modulate the expression of ANGPTL4 by tendon fibroblasts and which could, in future, be manipulated to influence tendon healing or adaptation.

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Novel functions of MCL-1 in ATM signalling, homologous recombination, and heterochromatin dynamics (2016)

MCL‑1 is a pro-survival member of the BCL-2 family of proteins that is over-expressed in a wide variety of human cancers. Beyond its canonical role regulating apoptosis, our lab was the first to describe an additional function of MCL‑1 in the nucleus where it is chromatin-bound at sites of DNA double strand breaks and potentiates DNA damage response signalling. This thesis further characterizes the nuclear functions of MCL‑1 and shows that it has a shorter protein half life in the nucleus compared to the cytosol. In response to low dose etoposide, MCL‑1-/- MEFs had diminished H2AX and pS824 KAP-1, while pS1981 ATM and pT68 Chk2 were lower across a 100-fold range of etoposide concentrations. Analysis of a panel of pathway-specific U2OS reporter cell lines determined that MCL‑1 participates in homologous recombination. Analysis of H2AX and RPA foci by immunofluorescence revealed that MCL‑1-depleted cells had elevated levels of RPA at 8 hours post-ionizing radiation but exhibited no difference in H2AX kinetics.A LC-MS/MS screen of endogenous MCL‑1 immunoprecipitations from etoposide-treated HeLa-S3 cells identified HP1 and p150CAF-1 as putative binding partners, which were validated by immunoblot and suggested a role for MCL‑1 in heterochromatin dynamics. MCL‑1 was found to bind HP1 and p150CAF-1 in the presence or absence of exogenous DNA damage, and was dispensable for the established interaction of HP1 and p150CAF-1. MCL‑1 was also not required for the localization of HP1, p150CAF-1, or KAP-1 to sites of DNA damage. MCL‑1 nevertheless had a functional role in promoting heterochromatin compaction as determined using the U2OS 2-6-3 cell line that has a quantifiable heterochromatin array. Furthermore, cells lacking MCL‑1 had reduced basal levels of H3K9me2/3. Taken together, I propose that MCL‑1 promotes heterochromatin compaction and H3K9me3 via novel interactions with HP1 and p150CAF-1. Other reports indicate that H3Kme3 leads to Tip60-mediated ATM activation following DNA damage, and that heterochromatic factors enhance downstream processes in homologous recombination. Therefore, MCL‑1 is capable of regulating numerous double strand break repair processes by influencing chromatin architecture.

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Polo-like kinase 1 as a prognostic and therapeutic target in high-grade brain tumors (2015)

High-grade brain tumors have some of the highest rates of cancer-related death. Occurring predominately in adults, patients with glioblastoma (GBM) are not expected to survive longer than two years. Similarly, medulloblastoma (MB) is the most commonly occurring malignant brain tumor in children and, although these cases have a much better probability of survival, the severe impact of high-intensity treatment often causes long-term negative side effects. Unfortunately, high-grade brain tumors are frequently resistant to standard treatments like temozolomide (TMZ). Further, the development of new drugs is hindered by the blood-brain barrier and the astronomical cost of drug discovery and clinical evaluation. The immediate need for new treatment options encouraged our approach of querying compounds that have previously been tested in clinical trials. Herein, we found that TMZ resistant GBM cells express high levels of the mitotic kinase, Polo-Like Kinase 1 (PLK1) and that TMZ resistance can be overcome using PLK1 kinase inhibitors, such as BI-2536. An assessment of off-patent drugs revealed that the anti-alcoholism treatment, disulfiram (DSF), also had efficacy in eliminating PLK1-high cells and this work proposes DSF can be repurposed for cancer treatment. The importance of PLK1 was further investigated in a retrospective study of MB patient samples that were assessed with the NanoString nCounter system. Cases with high PLK1 expression were more likely to relapse and had worse overall survival. This work suggests that stratification of these high-risk cases can identify patients that may benefit from PLK1 inhibitors, which cause G2/M arrest and apoptosis. Notably, both DSF and BI-2536 treatment had no negative growth effects on normal brain cells. Finally, translationally controlled tumor protein (TCTP) is a substrate of PLK1 that is used as a marker of kinase activity. An exploration of the clinical and mechanistic impact of TCTP demonstrated a striking association with the sonic hedgehog (SHH) MB subtype, as well, as establishing its role in cancer cell proliferation. In conclusion, the studies outlined in this thesis encourage the investigation of PLK1 as a therapeutic target in high-grade brain tumors and emphasizes the potential benefit of fighting cancer with repurposed drugs.

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Prognostic Role of BRAF in Human Cutaneous Melanoma: Gene versus Protein Expression (2015)

Melanoma is the deadliest type of skin cancer with an increasing incidence for past two decades. Once melanoma is metastasized (cancer cells are spread out through the body) there is no effective treatment available and 84% of the patients die within 5 years. However, the discovery of braf mutation in melanoma increased the hope for developing new treatments. We first evaluated the effect of braf V600E mutation on melanoma patient survival. In a systematic review we revealed that patients with braf V600E mutation have almost two times more risk of death compared with patients with wild type braf. Next we evaluated the correlation of brafV600E mutation with protein expression. We found that compared with nevi samples, BRAF protein expression was remarkably increased in primary melanomas and further increased in metastatic melanoma patients. Higher BRAF protein expression was significantly correlated with other poor prognosis factors and lead to a significant worse five-year survival. However, we did not find a significant correlation between BRAF protein expression and braf V600E mutation. In our attempt to investigate the cause of induced BRAF protein, we found novel expression of BRAF splice variants (BRAFsv) in both melanoma patients and cell lines. We identified new kinase-dead BRAFsv, which have a dominant negative effect on full-length BRAF and are able to suppress downstream signaling and reduce melanoma cell proliferation. These variants were highly expressed in primary melanoma compared to normal samples, while the expression was decreased in metastatic and more aggressive types of melanoma. In addition, kinase-dead BRAFsv showed a protective effect on patient survival, which remained significant at the presence of full-length BRAF. Thus, patients who expressed the kinase-dead variant and had lower levels of full-length BRAF expression showed the best survival rate in 5 years. Our invitro analysis also indicates that over expression of kinase-dead BRAFsv in melanoma cell lines enhances the effect of BRAF inhibitor treatment. All in all, the data presented in this thesis elucidated a new era in the evaluation of melanoma patient prognosis and revealed new possibilities for more effective melanoma treatments.

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Regulation of Macrophage Function Related to Atherosclerosis Development (2015)

Atherosclerosis has been identified as a chronic inflammatory disease resulting from interactions between immune cells and their microenvironment in the walls of susceptible arteries. Macrophages, critical players in innate immunity, participate in major events throughout all stages of atherosclerosis progression. Work in this dissertation is specifically interested in regulation of macrophage functions in the context of atherosclerosis. First, using bone marrow transplantation, we investigated how loss of eukaryotic elongation factor 2 kinase (eEF2K) activity affected atherosclerosis progression. Compared to mice transplanted with wild-type bone marrow, mice transplanted with bone marrow from eEF2K deficient mice had reduced atherosclerosis development after being fed with high-fat diet for 16 weeks. Impaired tumor necrosis factor-α release and subsequent adhesion molecule expression in the eEF2K inactive group may account for the reduction of atherosclerotic plaques. This finding suggested that the eEF2K inhibitor may be clinically useful to treat atherosclerosis. Second, we examined how oxLDL was involved in macrophage plasticity. We found that oxLDL polarized macrophages towards a novel subtype named MoL, which was characterized by high expression levels of heme oxygenase-1 and macrophage inhibitory cytokine-1. MoL cells are polarized, in part, through the activation of the PI3K/Akt pathway. MoL cells specifically up-regulates vascular cell adhesion molecule-1. This finding provided a more comprehensive view of macrophage plasticity in the context of atherosclerosis. Finally, we investigated signal transduction of ceramide 1-phosphate induced vascular endothelial growth factor release in macrophages. Using pharmaceutical inhibitors, we ruled out contributions of p38 MAPK and PKC-ζ signalling, and showed that the PI3K/Akt and MEK/ERK pathways were responsible for this process. Although we have no solid evidence to conclude on the mechanisms by which signals transduced from the outside of the cell to the inside, a rational hypothesis that this transduction requires ceramide 1-phosphate to be either embedded into, or actively transported through, the plasma membrane has been proposed. In summary, work in this dissertation contributes to our understanding of how macrophages functions are regulated by interacting with factors in the microenvironment. Results from this dissertation provide potential new avenues for discovery of novel therapeutic approaches to treat atherosclerosis.

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A Quantitative Proteomics Analysis of Human Cells Undergoing Apoptosis (2010)

Elucidating the events and mechanism of regulation of apoptosis is of wide interest to the scientific community, and to humanity, since apoptosis, so important for proper development and maintenance of an organism, is also responsible for disease when the process goes awry. In this thesis, a proteomics investigation into changes in protein concentrations and half-lives in early apoptosis is presented, enhancing our understanding of this process. Using Stable Isotope Labeling with Amino Acids in Cell Culture (SILAC), cytokine withdrawal-induced apoptosis of a human hematopoietic cell line, TF-1, was studied. This is a useful model in which signaling pathways regulating apoptosis have been extensively studied previously. A study such as this can be considered “hypothesis-generating”, but at the outset the hypothesis is that proteins whose functions are closely tied to regulation of apoptosis will show detectable changes in quantity in cells undergoing apoptosis.Initially three biological replicates were performed, comprising 200 samples in all, analyzed using an FT-ICR mass spectrometer. Relative abundance of 1451 proteins identified in common between three biological replicates was determined, and 124 proteins showing the largest concentration changes in response to cytokine withdrawal are discussed in more detail. A subsequent effort investigated protein half-life changes in response to cytokine withdrawal and identified 255 proteins for which half-lives were calculated. The apparent changes in protein half-life in response to cytokine withdrawal are discussed.A high level of coverage of the proteome was achieved, giving a large number of protein identifications and relative quantitations. Further I have been able to identify several apparently synchronous changes in concentration between proteins with related functions, suggesting possible interactions not previously described, or identified as playing a role in cell survival, proliferation or death. Further, I observed cytokine withdrawal-induced alterations in concentration in some proteins for which little is known. The proteomic analysis of apoptosis using SILAC to determine protein half-life data is also a novel approach. Together, the work in this thesis suggests numerous avenues of investigation potentially leading to novel findings regarding cells undergoing apoptosis; and also suggests a potentially fruitful avenue of investigation for clinical management of patients undergoing chemotherapy.

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Identification of a Novel Secretion System in Leishmania: Composition, Mechanisms and Immune Modulating Properties (2010)

Human infection with protozoa of the genus Leishmania results in a spectrum of disease manifestations collectively termed the leishmaniases. These diseases involve a chronic infection of macrophages which display a deactivated phenotype. Various proteins secreted by leishmania are known to interact with host signaling molecules, bringing about activation of negative feedback loops. Some of these have been shown to block interferon-γ signaling and to inhibit macrophage microbicidal functions. Unlike the well characterized secretion mechanisms used by bacterial pathogens, the mechanism(s) by which leishmania and other eukaryotic pathogens secrete proteins into host cells has remained elusive. The overall aim of this project was to gain a more thorough understanding of host immune-modulation by leishmania, based on the hypothesis that much of these effects are mediated by secreted proteins. The project goals were to: 1) comprehensively identify the proteins secreted by leishmania, 2) determine the mechanism by which proteins are secreted from leishmania into host cells, and 3) determine the functional properties of leishmania secreted compounds. To achieve these goals, a global proteomic analysis of leishmania secreted proteins was carried out using quantitative mass spectrometry. This identified 358 bona fide leishmania secreted proteins many of which were orthologs of proteins considered to be markers of mammalian exosomes. Subsequent experiments confirmed that leishmania secrete exosomes into conditioned media. Comparative proteomics showed that exosomes account for at least 50% of protein secretion by leishmania. Furthermore, the results showed that the cargo profile of leishmania exosomes is influenced by changes in temperature and pH, similar to those experienced by promastigotes after host invasion. Microscopy of leishmania infected cells confirmed the novel finding that leishmania use exosomes to deliver proteins into host cells. Additional studies demonstrated that leishmania exosomes have immunosuppressive properties which, in a cargo dependent manner, modulate the responses of monocytes, dendritic cells, and T lymphocytes. These findings suggest that leishmania utilize exosomes in long-range cellular communication and immune-modulation. In conclusion, this research has significantly advanced the current knowledge of leishmania biology, through the identification of novel secreted molecules, discovery of a secretion system, and description of the immune-modulating effects of leishmania exosomes.

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SPARC Enhances Chemosensitivity by Activating the Extrinsic Pathway of Apoptosis (2010)

Colorectal cancer (CRC) is the second leading cause of cancer death in Canada.Treatment failure in advanced disease is due to the development of chemotherapy resistance.Using a genomics approach, the Tai laboratory previously found that Secreted Protein Acidicand Rich in Cysteine (SPARC), a matricellular protein, was down-regulated in chemotherapyresistant CRCs. SPARC has tumour suppressor properties in ovarian and pancreatic cancers,where higher SPARC expression enhances apoptosis in vitro and tumour regression in vivo. InCRCs, it was found that exogenous SPARC re-sensitized CRCs to chemotherapy by inducingapoptosis and inhibiting tumour growth. In this thesis, the mechanisms of SPARC-mediatedapoptosis, the fragment of SPARC responsible for SPARC-mediated apoptosis and theinteraction between SPARC and collagen IV and its effect on chemosensitivity were examined.I demonstrated that SPARC can be internalized and interacts with the N-terminus of theprocaspase 8 death effector domain (DED)-containing domain, activating the extrinsic pathwayof apoptosis. This pro-apoptotic activity is mediated through SPARC’s N-terminus domain,where the N-terminus not only enhanced apoptosis in vitro, but also augmented tumourregression in vivo in combination with chemotherapy. The N-terminus domain of SPARC alsointerfered with the interaction between Bcl-2 and procaspase 8, decreased cell viability andincreased apoptosis. I also found that higher SPARC levels correlated with higher caspase 8expression. Further, I provided evidence that collagen IV and SPARC work in a co-operativemanner to enhance apoptosis. This thesis focuses on the interplay between SPARC/Bcl-2/procaspase 8 and collagen IV which may be important in modulating a tumour’s response tochemotherapy in CRCs, suggesting that SPARC may be a potential cancer therapeutic.

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Bad Serine 170 - regulation and cellular effects (2009)

The balance between cell proliferation and cell death is imperative for homeostasis inmulticellular organisms. This homeostasis had long been thought to be the result oftwo separate processes, but there is recent evidence indicating that the processes ofproliferation and apoptosis are coupled. Here we demonstrate that Bad, a proapoptotic member of the Bcl-2 family of proteins that is thought to exert a deathpromotingeffect by heterodimerization with Bcl-xL, is able to interact directly with the cell cycle machinery. Immunoprecipitation experiments indicate that Bad interactswith both Cdk2 and its late Gi cyclin partner, Cyclin E. This finding is relevant as we also demonstrate that prior to the conversion of Bad into a death factor; Bad’sphosphorylation state in healthy mammalian cells, specifically at Ser- 170, is able toinfluence cell cycle progression. Here we show that transfection with Bad Si 70A, amutant form of Bad which mimics the unphosphorylated form, results in a prolongedS phase during cell cycle. We also show that the kinase activity towards Bad Ser- 170increases in S phase of the cell cycle. Together this suggests that Bad Ser-170 is aphosphorylation site which is targeted during S phase and is able to interfere with the normal progression through S phase of the cell cycle. From this, it was of interest to elucidate the kinase responsible for phosphorylating Bad at Ser-170 as it may provide insight into signal transduction pathways that converge in terms of controlling both survival and cell proliferation, and ultimately cell expansion. Through a process ofcolumn purification, usage of chemical inhibitors, and gene knockdown, we showevidence that CaMKII-γ mediates the phosphorylation of Bad Ser 170, thusestablishing a novel connection between CaMKII signaling and apoptosis inhematopoietic cells. We hypothesize that CaMKII-γ plays a major role in controllingBad’s ability to induce apoptosis and to affect cell cycle progression, by controllingBad’s phosphorylation state at Ser-170.

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Investigation of the phosphatidylinositol 3-kinase pathway in B cells (2009)

There is hardly a cellular process that is not regulated in some way by phosphoinositides, which makes biochemical and physiological studies of these lipids extremely important. PI 3-kinases are key regulators of phosphoinositide metabolism and have been shown to affect a large variety of cellular responses. The key products of PI 3-kinases that have functional activity in higher eukaryotic cells are PI(3,4,5)P₃ and PI(3,4)P₂. PI(3,4,5)P₃ is universally accepted as one of the most important second messengers in signal transduction. However, our knowledge of the functions of PI(3,4)P₂ as a lipid second messenger is much less precise. In this dissertation, work was undertaken to elucidate the regulation of PI(3,4,5)P₃ and PI(3,4)P₂ production and downstream signaling in B cells. Cells with membrane targeted exogenous SHIP were utilized to manipulate phosphoinositide levels. The relationship of PI(3,4,5)P₃ and PI(3,4)P₂ levels to downstream PKB phosphorylation and activation was studied. PI(3,4,5)P₃ and PI(3,4)P₂ levels were found to closely correlate with PKB phosphorylation levels at Thr308 and Ser473, respectively. In addition, PI(3,4)P₂ levels determine the PKB activity in the cytosol; while PI(3,4,5)P₃ levels determine PKB activity at the plasma membrane. Different doses and different forms of B cell receptor (BCR) agonists were used for stimulation. PI 3-kinase activation was studied carefully following stimulation with low doses of anti-BCR antibody and F(ab')₂ fragments. Low concentrations of F(ab')₂ fragments produced higher levels of PI(3,4,5)P₃ than did a high concentration of F(ab')₂ fragments. Downstream PKB signaling was studied in these models. Similar conclusions were drawn from both SHIP over-expressing BJAB cells and dose-dependent BCR stimulations. We speculated that phosphoinositides’ regulation of the kinetics of PKB phosphorylation at Ser473 and Thr308 might be mediated by additional proteins. Investigation of plasma membrane-associated PKB showed that it formed a protein complex of around 400KD, which we attempted to characterize further with respect to PKB phosphorylation and association with lipids. In conclusion, phosphoinositide production is intricately regulated in vivo to control downstream signaling. The levels of PI(3,4)P₂ and PI(3,4,5)P₃ have precise and profound effects on PKB and other molecules such as TAPP and Bam32. This study has contributed new insight into the PI 3-kinase signaling pathway from the aspect of phosphoinositide lipid function.

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Oxidized low density lipoprotein-mediated macrophage survival : a role for calcium and regulation of cellular energy (2009)

Oxidized low density lipoprotein (oxLDL) as well as specific macrophage populations, play a pivotal role in the initiation and progression of atherosclerotic lesions. Our group previously reported that oxLDL inhibits apoptosis in bone marrow-derived macrophages (BMDM) deprived of macrophage colony-stimulating factor (M-CSF). In this study, I showed that oxLDL induces an oscillatory increase in intracellular calcium ([Ca²+]i) that is mediated by the activation of sphingosine kinase. This leads to activation of the Ca²+/calmodulin dependent kinase, eukaryotic elongation factor-2 kinase (eEF2 kinase). Both the increase in [Ca²+]i and activation of eEF2 kinase can be blocked by BAPTA-AM, an intracellular Ca²+ chelator. Addition of oxLDL also results in the phosphorylation of eEF2, the only known substrate of eEF2 kinase. The eEF2 kinase selective inhibitors, TS-4 and TX-1918, blocked oxLDL-mediated phosphorylation of eEF2 as well as oxLDL’s ability to promote survival of BMDMs. eEF2 kinase can be negatively regulated by p38 MAPK. Withdrawal of M-CSF results in the activation of p38 MAPK, an effect that is blocked with the addition of oxLDL. This indicates that oxLDL can positively regulate eEF2 kinase activity by both (1) generating an oscillatory increase in [Ca²+]i and (2) inhibiting its negative regulation by p38 MAPK. eEF2 is a monomeric GTPase that regulates peptide chain elongation and its phosphorylation inhibits its activity. Addition of oxLDL results in a decrease in overall protein synthesis and induction of autophagy in BMDMs. This suggests that under conditions of metabolic stress (e.g., growth factor withdrawal), there may be an eEF2 kinase-dependent protective mechanism that can be activated by the presence of oxLDL, thus linking energy conservation (e.g., via inhibition of protein synthesis) and the replenishment of energy supplies by digestion of cellular organelles through the induction of autophagy.

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Tendon overuse pathology : clinical and laboratory studies (2008)

Background: Painful tendon overuse pathology (tendinosis) is poorly understood. Theobjectives were to identify major cell populations within clinical tendinosis lesions, andto examine factors involved in the regulation of tendon cell death, survival, orproliferation. The overarching hypothesis was that both cell death and cell proliferationplay roles in the development of tendinosis.Methods:1: Chronic patellar tendinosis tissue was compared with normal, pain-free patellar tendonusing Western blot, immunohistochemistry and in situ hybridization. A variety of celltypes were examined in relation to relevant features of soft tissue injury and repairincluding cellular proliferation and versican expression.2: In adult male rats, early tendinosis was induced in the supraspinatus tendon by 4-16weeks of mechanical loading (eccentric exercise). Tendons were analyzedmorphologically using polarized light and transmission electron microscopy, and byimmunolabeling for molecular markers of proliferation and survival.3: The influence of IGF-I on tenocyte survival was tested in response to chronic hypoxiain a cell-culture setting.Results1: Tendinosis was characterized by proliferation of tenocytes, endothelial cells, andsmooth muscle cells within a versican-enriched extracellular matrix. Mast cells were alsomore numerous in patient biopsies, whereas macrophages and lymphocytes were virtuallyabsent. VEGF expression was increased in endothelial cells from tendinosis tendons andwas more marked in patients with shorter symptom duration.2: Mechanical loading of the rat supraspinatus tendon by downhill running caused focaltendon lesions characterized by tenocyte proliferation, collagen disarray andglycosaminoglycan accumulation. Tenocytes in these areas of injury demonstrated aproliferative response which correlated with IGF-I expression and phosphorylation ofERK-l/2and IRS-1.3: Prolonged hypoxia of primary tenocyte cell cultures resulted in tenocyte apoptosis andcaspase activation. Apoptosis could be prevented dose-dependently by IGF-I, whichactivated the PKB survival pathwayConclusionsThe current studies outlined predominant cell populations present in tendinosis lesionsand identified factors which may be involved in regulating their death, survival andactivity. These experiments have opened up new avenues of research into thepathophysiology of tendinosis.

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