Relevant Thesis-Based Degree Programs
We conduct translational cancer research and have various ongoing projects focusing on Pancreatic Cancer. We are looking for students interested in a bioinformatics and bench top project studying genomic alterations and rearrangements and students interested in the development and use of patient deterived organoid models for translational research including drug screening, metabolism, and idetification of treatment markers.
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.
ADVICE AND INSIGHTS FROM UBC FACULTY ON REACHING OUT TO SUPERVISORS
These videos contain some general advice from faculty across UBC on finding and reaching out to a potential thesis supervisor.
Graduate Student Supervision
Master's Student Supervision
Theses completed in 2010 or later are listed below. Please note that there is a 6-12 month delay to add the latest theses.
Pancreatic ductal adenocarcinoma (PDAC) can be stratified into distinct transcriptomebased molecular subtypes, with the ‘basal-like’ (or ‘squamous’) subtype being associatedwith worse prognosis, compared to the ‘classical’ subtype. These subtypesare assigned based on Moffitt genes signature scores where scores above a thresholdvalue are indictive of the basal-like subtype. Furthermore, PDAC tumours have uniquemetabolic transcriptomic profiles based on stratification of glycolytic and cholesterogenicgenes which correlate with basal-like and classical gene expression patterns,respectively. The mitochondrial pyruvate complex (MPC) mediates the transport ofpyruvate into the mitochondria. The mitochondrial pyruvate carrier 1 (MPC1) gene,which encodes one of two subunits of MPC, is deleted in over 60% of metastatic PDACand PDAC glycolytic tumours have lowest levels of MPC1 expression. Using PDACtissue microarray data, our group found that reduced MPC1 protein expression correlateswith reduced survival in patients. Therefore, we hypothesized that targetingMPC1 will alter metabolic reprogramming which may modulate tumour aggressivenessin tumour models. Genomically and clinically annotated patient-derived tumourorganoids (PDOs) were generated from metastatic biopsies from patients enrolled inthe PanGen study. Baseline metabolism and metabolic flux were measured usingSeahorse XFe96 based glycolytic and mito stress tests, these testswere adapted for compatibilitywith PDOs. Baseline glycolysis and oxidative phosphorylation (OXPHOS)rates demonstrated high variability in glycolytic reserves highlighting the extent ofmetabolic reprogramming in PDOs. This variability in glycolytic reserve positivelyassociated with Moffitt gene signature scores where PDOs with larger reserves tendedto have higher Moffitt scores. To alter metabolic activity, eight PDOs were treated for48 hours with UK-5099, a MPC1 inhibitor, or SRT-1720. SRT-1720 is an activator ofsirtuin 1 (SIRT1) which deacetylates peroxisome proliferator-activated receptor gammacoactivator 1-alpha (PGC1?), enhancing its activity. PGC1? has been shown to increasetranscription of MPC1. Treatment with UK-5099 raised glycolysis and glycolyticcapacity in four PDOs tested and reduced maximal respiration rates in seven PDOs.Treatment with SRT-1720 reduced glycolytic capacity in two PDOs but did not alter OXPHOSrates. Taken together, these results elicit the variability in metabolic dependencyin PDOs to meet energy demands and the plasticity of metabolic reprogramming.
Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal forms of cancer, with a 5-year survival rate of less than 10%. Current challenges include limited therapeutic options and lack of biomarkers that predict treatment response. Therefore, I sought to determine if a recently rediscovered treatment, pharmacological vitamin C, has clinical utility in PDAC. I determined that PDAC cell lines have differential sensitivity at doses tested. Previous research in colorectal cancer indicated that KRAS mutations infer vitamin C sensitivity, which was a trend in my results. Therefore, I created two isogenic cell line models expressing either KRAS G12D or KRAS G12V. Testing depicted increased sensitivity in one model but none others, suggesting that factors beyond oncogenic KRAS alone may be needed to increase sensitivity to vitamin C treatment. Oncogenic KRAS is known to increase glycolysis through the Warburg effect. Interestingly, pharmacological vitamin C treatment is also hypothesized to affect this pathway. Therefore, I sought to determine the relationship between vitamin C and glycolysis to determine potential markers of vitamin C sensitivity. Testing glycolysis rates demonstrated that vitamin C inhibits glycolysis independent from vitamin C toxicity. Work by Daemen et al. identified that glycolytic inhibitors cause toxicity selective to glycolytic dependant cells, whereas lipogenic cells survive. Furthermore, they characterized our two vitamin C sensitive cell lines as glycolytic. To further understand if glycolytic dependence influences vitamin C sensitivity, I used glucose withdrawal to reduce the cell’s glycolytic dependence. In low glucose conditions, higher doses of vitamin C were needed compared to high glucose conditions, suggesting that glycolytic dependence does influence toxicity to vitamin C. Together, my results suggest that glycolytic dependence may be a good marker for determining vitamin C sensitivity.To test if vitamin C is toxic in KRAS mutated patient-derived models, PDAC-derived organoids were created and treated using vitamin C monotherapy and combination therapy with gemcitabine. Vitamin C showed toxicity as a monotherapy and increased toxicity when combined with gemcitabine. This is the first known use of organoids in testing vitamin C treatment and suggests, congruent with other research, that vitamin C alone and in combination has clinical utility.
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