THIS COMPETITION IS CURRENTLY CLOSED
Two $25,000 fellowships are offered by Mr. Roman M. Babicki. The awards are to support doctoral candidates in any academic department, provided that their supervisor has a primary appointment in the Faculty of Medicine. Candidates must be undertaking cancer research and be either Canadian Citizens or Permanent Residents. Awards may be renewed for a second consecutive year, but no individual or project will receive support from this fund for more than two years. The awards are made on the recommendation of the Faculty of Medicine in consultation with the Faculty of Graduate and Postdoctoral Studies.
$25,000 for one year. Holders of the award may re-apply for a second year.
Applicants must be registered as full-time students in a doctoral program at UBC and have already advanced to candidacy. Applicants must be either Canadian Citizens or Permanent Residents of Canada. Applicants must be in good academic standing, and conducting cancer research under the supervision of a UBC faculty member who has a primary appointment in the Faculty of Medicine. Candidates cannot have received support from this fund for more than two years.
A completed application consists of:
2. Post-secondary transcripts from all post-secondary institutions attended
Copies of transcripts are accepted, but must be initialed by the candidate’s supervisor. Initialing of official sealed transcripts is not required. Electronic copies are also accepted, and do not require initialing if sent directly from the applicant’s graduate program assistant.
3. Letters of support from two sponsors
One letter should be from the proposed or current supervisor of the candidate, and the other from an individual familiar with the candidate’s academic and research abilities. Sponsors should be asked to comment on the candidate’s research potential and achievements, interpersonal skills, academic abilities, and greatest strengths and weaknesses. Electronic copies of letters of support are accepted if sent directly from the sponsor.
Complete applications need to be received by: Likely mid-July, 2017–date TBA
Transcripts and letters of support should be submitted to:
Dr. Wendy Robinson, Assistant Dean, Graduate and Postdoctoral Education
c/o Heather Muckart
317-2194 Health Sciences Mall
Vancouver BC, V6T 1Z3
Please refer to the Guidelines and FAQs for specific formatting and submission details.
Hye-Jung (Elizabeth) Chun’s research focuses on malignant rhabdoid tumours (MRTs), which are childhood cancers that resist known chemotherapies and spread quickly to other areas of the body (i.e. metastasis). MRTs arise frequently in kidneys and the brain, but the cell type that gives rise to MRTs is currently unknown, which poses challenges in understanding molecular aberrations that can be therapeutically targeted. Despite MRT’s highly malignant characteristics, loss of a protein called SMARCB1 is responsible for MRT development. Characterizing molecular profiles of MRTs is important to understand mechanisms behind the pathology of this fast-progressing cancer type. To date, her research has revealed surprising molecular diversities in MRTs that resulted from SMARCB1 loss, and indicated dysregulation of developmental pathways, particularly those of embryonic stem cells and neural crest cells, a putative cell type of origin for MRTs. The data generated from her research and the observations made from her analyses contribute to enhanced understanding of MRT biology, which she hopes will ultimately aid in development of better therapies for MRT patients.
Haolong Li studies advanced prostate cancers, the primary treatment for which is castration therapy, which in turn inhibits the actions of a protein inside cancer cells known as the androgen receptor (AR). There are several AR inhibitors used in clinical practice that can effectively delay tumor growth. Unfortunately, such benefits only last for a short period of time. Tumors eventually find alternative ways to re-activate AR activity. Previous studies show that AR requires another protein called Topo II to start its function. His new studies further indicate that Topo II inhibitors can block AR function and suppress prostate tumor growth including the drug resistant tumors. To get the ideal Topo II inhibitors that have higher efficiency and lower toxicity than the current ones, Haolong has co-developed a computer-aided drug screening system to target Topo II. Higher scored compounds evaluated from the system exhibit better performance in biological tests, proving the accuracy and precision of the whole screening process. Therefore, he now propose using this established system to screen up to 100 million compounds for new generation Topo II inhibitors and ultimately for treating prostate cancer patients.
Karissa Milbury researches Dis3, an enzyme that is commonly mutated in the blood cancer multiple myeloma. Dis3 acts as an RNA supervisor in the cell: it helps process RNA to make sure it is transported to the right place, and it degrades RNA that has been created inappropriately or outlived its usefulness. Her research group has found that mutations that cripple Dis3 also cause RNA to get stuck to the DNA, creating damage-prone structures called R-loops. She aims to identify why and how Dis3 affects R-loops, because this would directly link a mutation seen in multiple myeloma with the DNA damage that makes cancers dangerous.
Ling-I Olivia Tseng researches the associated risk of osteoporosis in some forms of breast cancer treatment. Her work has shown that osteoporosis screening rates are still below 30% for women treated for breast cancer in British Columbia. Patient notices with information packages have been shown to increase osteoporosis screening rates from 22% to 51% for patients with prior fractures. However, it is unclear whether information packages can improve osteoporosis screening for women with a prior breast cancer history. A research study has been designed to answer this research question. Before conducting a large-scale study, her research group is conducting a pilot study to determine: 1) the acceptance of the study procedures and 2) the willingness of participating in this study among women with a prior breast cancer history. This study can potentially help family doctors identify women with elevated risk of fractures in this unique group.
As a Ph.D. candidate in the department of Pathology and Laboratory Medicine, Jay Gunawardana studied malignant lymphomas, the fourth most frequent type of cancer in men and women that affects patients of all ages. Lymphomas are diverse in their biology and clinical behaviour and unfortunately, the current standard of care fails to eliminate it in a substantial proportion of patients who are then very likely to succumb to their disease. The causes for these unfavorable clinical outcomes are partly due to the lack of novel therapeutic targets.
Dr. Gunawardana’s work focused on improving the survival of patients with a specific type of lymphoma, called primary mediastinal large B-cell lymphoma (PMBCL). Along with his research team, he discovered novel mutations in a subset of PMBCL patients that activates oncogenic signaling ("JAK-STAT signaling") and leads to aberrant PMBCL tumour cell signaling and tumor growth. He also examined how these gene mutations contribute to the formation of these cancers and how knowledge about JAK-STAT signaling can help identify drug targets to improve therapies for affected patients. Ultimately, he hopes his findings will provide a rational therapeutic target for future treatments; maximizing cure rates and minimizing treatment-related side effects.
Mani Roshan-Moniri is a PhD candidate in Experimental Medicine Program, in the department of Urologic Sciences. Mr. Roshan-Moniri’s work focusses on understanding the mechanism of action of candidate drug compounds for prostate cancer that targets the distinct protein ETS-related gene (ERG). Over 50% of all prostate cancer involves a genomic irregularity in the ERG. This alteration results in the overexpression of ERG in the prostate where it acts to promote disease metastasis. Androgen deprivation therapy (ADT) acts by inhibiting the production of androgens or by blocking the interaction of androgens with androgen receptors, and it is the standard treatment for locally advanced, recurrent and metastatic prostate cancer. However, it is only initially effective, as resistance to ADT often occurs. Mr. Roshan-Moniri therefore aims to develop candidate anti-ERG compounds as an entirely new generation of therapeutics that could either supplement or replace the conventional resistance-prone androgen deprivation therapy for metastatic, castration-resistant prostate cancer patients