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Home | BC | Your Dollars At Work | Fellowships | 2014-2015 Annual Doctoral and Post-doctoral Fellowship Grant Recipients

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2014-2015 Annual Doctoral and Post-Doctoral Fellowship Grant Recipients

Hildur Knutsdottir, University of British Columbia, Vancouver


Project Title
 
Modelling interactions of breast tumor cells with their microenvironment
 
Project Overview
 
The focus of this project is on the interactions between breast cancer cells, immune cells and blood vessels, and the role they play in metastasis. Evidence suggests that observing these cells in close proximity to each other is a marker for a metastatic disease.
 
Dr. Hildur Knutsdottir intends to characterize and quantify the details of the signalling that mediates cancer cell - immune cell - blood vessel interactions. Furthermore, he will investigate how manipulating this signalling affects the cancer cell migration to identify potential drug targets. To study these signalling interactions he has developed a computational model based on physical and mathematical principles. The model is three-dimensional (3D). It simulates cells as individual entities and calculates signalling chemical concentrations. All model assumptions and parameters are determined in close collaboration with experimentalists to ensure their physical relevance. Using this model Dr. Knutsdottir will be able to quantify the effects of each system parameter on cancer cell migration. The parameter (or combination of parameters) that significantly affect the cancer cell migration can be considered as potential targets in drug development. The identification of these drug targets will be the novel contribution of this project to advancing breast cancer research towards a future without metastatic risk.

Jagbir Singh, University of British Columbia, Vancouver


Project Title
 
Development of lipid-based nanoparticulate hydroxychloroquine formulations for use in combination with autophagy inducing drugs for treatment of metastatic breast cancer
 
Project Overview
 
Metastatic breast cancer (MBC) is a leading cause of mortality in women with breast cancer. Treating patients with MBC is a real challenge because the cancer is growing in multiple locations and the cancer cells that give rise to MBC are ones that have survived previous treatments and are therefore insensitive to the drugs that were used previously. Insensitivity is due in part to the fact that the cancer cells develop survival mechanisms that effectively protect them for the action of selected drugs. It is possible to improve the sensitivity of these cancer cells towards known anti-cancer drugs by combining these drugs with other drugs that specifically target the survival mechanisms that exist in these cancer cells.
 
In Dr. Jagbir Singh’s research, he will use one such drug that has been used in the past to treat malaria, but is now being re-purposed for use in the treatment of cancer. As noted above, MBC is a disease where the cancer is growing in multiple sites; like the bone, brain and lung. Dr. Singh will develop formulations that are designed to ensure that the drug used is delivered to different sites where MBC grows. These studies will generate data that will help decide which formulation provides the best treatment outcomes as determined in animal models of MBC; studies that provide the first step towards development of treatments suitable for testing in patients with MBC.
 

Jerry Tien, BC Cancer Agency, Vancouver

Project Title
 
Targeting the regulation of DNA repair by CDK12 for breast cancer therapy
 
Project Overview
 
There are two main pathways that repair severe DNA damage, and mutations in these pathways are frequently found in breast cancer cells. Recent studies show that tumours with mutations in one pathway can be effectively treated with drugs that inhibit the other pathway. Understanding the function of both pathways in cancer will therefore benefit the development of new therapies. Recent evidence suggests that a protein named CDK12 is a regulator of one pathway, and mutations in CDK12 have been found in breast tumours. Preliminary results indicate that CDK12 likely regulates an essential cellular process termed “alternative splicing,” where gene segments are assembled in the correct order. Therefore, Dr. Jerry Tien has hypothesized that CDK12 controls the alternative splicing of genes in DNA repair. He will examine the effect of CDK12 mutations on alternative splicing after DNA damage. Dr. Tien will also identify mutations in the other repair pathway that render cells susceptible to CDK12 inhibitors. Together, these results will reveal how errors in the repair processes regulated by CDK12 can lead to tumour development and define the population of breast cancers that can be treated with CDK12-based therapy.
 

Kriti Singh, University of British Columbia, Vancouver

Project Title
 
The development of anti-estrogens targeting the Activation Function 2 site of Estrogen Receptor Alpha as potential therapeutics for hormone resistant and metastatic breast cancer
 
Project Overview
 
Breast cancer (BCa) is the leading cause of cancer related death in women worldwide. Tamoxifen (Tam) is used to treat women with estrogen receptor alpha positive (ERα+) BCa. But the effectiveness of such treatment is usually temporary due to progression of surviving tumor cells to the resistant state. ERα expression is retained in the majority of the resistant and metastatic BCas. Therefore, Dr. Kriti Singh’s proposed research aims to develop alternative therapeutics targeting ERα with a unique mechanism of action by combining methods of modern computational drug design with extensive biological validation. The best leads will be tested in xenograft models. Their potential synergistic effects in combination with known therapeutics will be evaluated in Tam resistant models.
 
These preclinical studies will provide the platform for advancing the compounds into clinical testing. Dr. Singh’s team anticipates that their compounds will overcome the limitations of current therapies and prolong patient survival after development of resistance, thereby significantly improving the quality of life. This work will greatly advance the Foundation’s vision of creating a future without breast cancer.
 

Lindsay DeVorkin, BC Cancer Agency – Deeley Research Centre, Victoria

Project Title
 
Investigating the role of autophagy in the breast tumour microenvironment and its implications in anti-tumour immunity
 
Project Overview
 
Tumours are situated within a hostile, nutrient and oxygen-deprived microenvironment where they activate a mechanism called autophagy to promote cancer cell survival. Although the immune system is capable of identifying and destroying cancer cells, the tumour microenvironment can enhance or weaken immune responses, and it can also activate autophagy as a means of immune escape. In a preliminary study Dr. Lindsay DeVorkin’s team found that mice with a defect in autophagy were significantly impaired in their ability to form breast tumours. This impairment was associated with increased tumour-associated immune cells. They hypothesize that autophagy inhibition in breast cancer will enhance the anti-tumour immune response by altering the tumour microenvironment. This study will be carried out using mouse models of breast cancer as well as human breast cancer specimens. The proposed research will contribute significantly to the understanding of how autophagy and the immune system interact and how it correlates with treatment response and patient outcome. Moreover, this work will identify a potential new way to enhance the immune response to eradicate breast cancer more effectively.
 

Tony Lok Heng Chu, University of British Columbia, Vancouver

Project Title
 
Understanding and targeting aurora kinase A activity during the migration and metastasis of triple negative breast cancers
 
Project Overview
 
Breast cancer is the second leading cause of cancer death in Canadian women and metastasis (or movement) to other tissues of the body is the principal cause of death. Normal cells in the breast do not move and Dr. Tony Lok Heng Chu believes that a breast cancer cell gains the ability to move by activating a certain pathway, which alters the cell’s internal skeleton. This pathway is controlled by an enzyme called aurora A kinase (AURKA) and the goal of Dr. Chu’s research is to better understand how this pathway controls the movement of breast cells, what other regulatory molecules are involved to activate the kinase, and how this pathway can be targeted with new drugs.
 
His project will examine this molecular pathway using a number of breast cancer cells that grow indefinitely in the lab. To better understand the process of metastasis, Dr. Chu will transfer these cells into mice and follow the growth and movement of tumor cells based upon their bioluminescence. Finally, he has examined a large array of human breast cancer tissues for the abundance of a marker for AURKA activity to determine whether this marker predicts the patient’s long term survival and response to therapies. The results from Dr. Chu’s studies will provide a more complete understanding of the process of breast cancer metastasis and determine whether new drugs that target AURKA may be effective at preventing the movement of breast cancer throughout the body.