Our People
Awardees
![]() Medhi Amiri |
I received my B.Sc degree in Cellular and Molecular Biology from University of Tehran, Iran. I am currently working toward my M.Sc at the University of Western Ontario in the lab of Dr. Fred Dick. Our lab studies the role of the Retinoblastoma protein (pRB) in cancer and development. pRB is a key regulator of cell proliferation in the G1 phase of the cell cycle. There are many protein partners which cooperate with pRB to act as a tumor suppressor. TGF-β induces G1 growth arrest by inhibiting CDK activity which leads to dephosphorylation and activation of pRB. Our lab uses a knock-in mouse that carries a three amino acid substitution mutant to disrupt the LXCXE cleft in pRB (called Rb1ΔL). Previously, we showed that TGF-β mediated growth arrest is defective in Rb1ΔL mice and pRB`s ability to repress transcription of E2F target genes is lost. This indicates pRB-LXCXE interactions are uniquely needed for TGF-β mediated cell cycle arrest. My project, uses these mice as an in vivo model together with a cell culture system to study pRB-LXCXE interactions in TGF-β growth arrest and to determine the role of the TGF-β-pRB pathway on the initiation of mammary tumors.
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Navid Baktash completed his Bachelor’s degree in Medical Sciences at the University of Western Ontario and is currently in his first year of his MSc, in the department of medical biophysics supervised by Dr. John Lewis. The ability of cancer cells to recruit vasculature and migrate is
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Matthew Cecchini Matt's current research is investigating the role of the E2F1 specific binding site in the retinoblastoma tumour suppressor. |
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Di Chen My research interest: Hypoimmune response is a major hurdle for most immune anti-cancer therapies. Indoleamine 2, 3-deoygenase (IDO) is an immunosuppressive molecule that inhibits anti-cancer immunity. We hypothesize that knockdown of IDO using siRNA will enhance dendritic cel (DC)-based immune therapy for breast cancer. My aim in this program: (1) Develop a method to deliver siRNA targeting IDO to DCs (2) Assess how well mobilized CDs with siRNA-silenced IDO inhibit or abrogate the growth of tumour cells in immunocompetent host mice, and (3) If Aim 2 reveals enhanced capacity to inhibit the growth, I will explore the mechanisms underlying anti-cancer immunity mediated by DCs with siRNA-silenced IDO. Through the Strategic Training Program, I hope to expand my research horizons to include new knowledge and technical skills in pre-clinical cancer research, cancer imaging, anti-cancer therapy and pharmacokinetics - this requires interaction with other trainees and primary investigators across different laboratories. This cross-disciplinary training will be an asset for my future career as a successful cancer researcher. |
Choi-Fong Cho |
Choi-Fong Cho |
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Jenny Chu
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![]() Michael Cohen |
Michael Cohen
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Rohann Correa |
Rohann Correa Research Interest: |
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Courtney Coschi The retinoblastoma protein (pRb) belongs to the pocket protein family and is a tumor suppressor, which plays a role in cell division cycle control. pRb contains an LXCXE binding cleft, which is its most highly conserved region across species and other pocket proteins. To determine the importance of the LXCXE cleft, our lab has made a mouse such that the cleft on pRb is mutated and therefore is incapable of binding proteins with the LXCXE motif. Based on recent data, I hypothesize that the LXCXE binding cleft on pRb is required both for proper centromere function and chromosome architecture during mitosis; without which, there will be genome instability, enabling cancer formation. |
Niamh Coughlan |
Niamh Coughlan |
![]() Alysha Croker |
Alysha Croker There is some evidence to suggest that breast stem cell-like cancer cells (or “cancer stem cells”) preferentially survive cancer therapy. Since these stem-like cells also have a high capacity to initiate and sustain tumour growth; therefore, it is possible the stem-like cells left behind following therapy are responsible for tumour relapse. My experimental results to date indicate that that these stem-like breast cancer cells can survive about 4-5 times better than the non stem-like tumour cells after receiving either radiation or chemotherapy. Interestingly, when cells are first incubated with all-trans retinoic acid (ATRA), a differentiation agent, the stem-like cancer cells become significantly more sensitive to therapy. I am currently investigating what might be making these stem-like cells so resistant to therapy, and why the ATRA makes the stem-like cells more sensitive to therapy. Thus far I have observed that the stem-like cells have a higher expression of two proteins called p-glycoprotein and GSTpi which play an important role in therapy resistance. By demonstrating how stem-like breast cancer cells resist current breast cancer therapies, our studies could potentially identify new targets for eliminating the most dangerous cells within the tumour, thus leading to more effective ways of treating breast cancer. |
Donna Cvetkovic |
Donna Cvetkovic Research Interests: Over a decade ago a new metastasis-suppressor gene was identified and named KISS1 gene, although, it was not until 2001 that the peptide products of KISS1, the kisspeptins (KP), were identified as the endogenous ligands for the KP receptor (KISS1R). The anti-cancer activity of the KP system has been identified in thyroid, ovarian, bladder, gastric, esophageal, pancreatic, and lung cancers. Nevertheless, the role of KPs in breast cancer has been difficult to discern. Our recent studies have demonstrated for the first time that KP-10, the most potent kisspeptin, stimulates the migration and invasion of estrogen-receptor negative human breast cancer MDA-MB-231 and Hs578T cells (that endogenously express KISS1R) by transactivating the epidermal growth factor receptor. However, whether or not KISS1R signalling is directly required for metastasis is unknown and will be investigated here. |
Stefanie De Jesus |
Stefanie De Jesus |
Christine DiCresce |
Christine DiCresce |
Dylan Dieters-Castator |
Dylan Dieters-Castator Dylan Dieters-Castator completed his BMSc in Biochemistry and Cell Biology at the University of Western Ontario and is starting his Master’s degree in Dr. Lynne-Marie Postovit’s lab. |
![]() Brandon Disher |
Brandon Disher Using X-ray computed tomography (CT), it is possible to map the attenuation characteristics of different materials in three dimensions (3D). The measured pixel attenuation values are expressed in units of CT Numbers (Hounsfield Units or HU). This procedure is commonly used in medical diagnostic imaging for cancer radiation therapy. In addition to qualitative imaging, accurate material density information can be derived from the CT Numbers. Such quantitative densitometry is used in cancer radiation therapy for computing dose deposited within patients exposed to an external beam of ionizing radiation. As opposed to older simpler systems, CT images, obtained from modern wide-beam systems, such as multi-slice or Cone Beam CT (CBCT), may contain erroneous CT numbers, which appear as physical artifacts in the images. These artifacts, or apparent flaws in derived density, can be caused by photon noise, x-ray spectral effects, atomic number variations of the absorbing materials, object motion during scanning, and detection of scattered X-rays which is accentuated with broad-beam imaging. Incorrect CT number measurement will distort dosimetric computations, which can lead to under or over dosing of regions within the exposed patient. Thus, the goal of my PhD is to study modern CT scanners, to quantify the error in density information and images produced by these new systems, and to measure the impact of this error on dosimetric computations. The London Regional Cancer Program (LRCP) is an ideal location for conducting my research. There is established expertise in quantitative densitometry, radiation dosimetry, and 4D-CT (3D-CT at multiple phases of the breathing cycle). As well, the LRCP is equipped with the most modern CT scanners and dose planning software. |
Stephanie Dorman |
Stephanie Dorman Her project involves designing diagnostic DNA probes that are targeted specifically to regions that will be informative for breast cancer patient care. It is now common in breast cancer diagnosis to characterize tumours using genome-wide assessments, establishing which genes have been altered, amplified, or deleted. In addition to genetic irregularities that are commonly tested for, the probe designs will determine the status of stable genetic targets of chemotherapy agents. The breast cancer focused designs provide an opportunity to reduce costs of diagnostic testing while allowing personalized treatment decisions to be made. |
Vasiliki Economopoulos Vasiliki is currently working on her doctorate at the University of Western Ontario in the department of medical biophysics. She also completed a Bachelor’s of Engineering Science degree in the same location. |
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Malek Hannouf |
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Ernie Ho Melanomas are aggressive and metastatic cancers accounting for 80% of all dermatological cancer deaths, yet no effective treatments for advanced or metastatic forms of this disease exist. Integrin-linked kinase (ILK) is a scaffold protein involved in cell migration and invasion. Elevated ILK expression is frequent in invasive melanoma, and correlates with poor prognosis and < 5yr patient survival. The molecular mechanisms by which ILK regulates these processes are poorly understood. We have identified a novel complex containing ILK and ELMO2, another key regulator of migration and showed that ILK and ELMO2 cooperate to promote cell migration. However, the contribution of ILK:ELMO2 complexes to migration and invasion of melanoma cells has yet to be explored. Modulation of ILK-ELMO2-mediated migration and invasion may provide new therapeutic tools against melanoma, a tumor type with high mortality and currently poor treatment options. |
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Michael Jewer He is currently a PhD student in the Department of Anatomy & Cell Biology in the laboratory of Dr. Lynne-Marie Postovit. His research examines the potential mechanisms through which low oxygen regulates the embryonic morphogen Nodal in poorly metastatic breast cancer. |
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Amy Kossert Her research interests are focused primarily on the development and implementation of exercise interventions to complement cancer prevention and treatment efforts. Amy is particularly interested in exercise training throughout the disease trajectory as a means of mitigating the negative psychological consequenses associated with cancer. |
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Lori Lowes The majority of cancer related deaths are from metastatic disease, which is often correlated with the presence of circulating tumour cells (CTCs) in the blood. It has been shown that greater than 5 CTCs in 7.5ml of blood correlates with significantly lower rates of overall survival. The development of the CellSearch System (CSS) by Veridex has allowed for the sensitive detection and quantification of these rare CTCs. The purpose of my project is to use the CSS to quantify and characterize CTCs with respect to molecular markers of interest in human blood samples. In particular the cancer stem cell marker CD44, a marker of cell death M-30, and the clinically significant prostate cancer marker, prostate-specific antigen (PSA). Once properly optimized the CD44 marker will be an important tool in studying cancer stem cells and in developing a better understanding of the metastatic cascade. In addition, the M-30 protocol could be exploited as a tool to measure the effectiveness of therapy. Finally, the PSA marker could be utilized to examine the expression of PSA in CTCs of prostate cancer patients. |
![]() Saman Maleki-Vareki |
Saman Maleki-Vareki received his M.Sc. in Microbiology from the University of Isfahan (Iran). He is currently working on his Ph.D. at The University of Western Ontario under the supervision of Dr. Mansour Haeryfar. His research interest involves the improvement of anti-tumor CD8+ T cell responses. These T cells are one of the main effector cells of the adaptive immune system, and can recognize and eliminate tumor cells in a highly specific manner. Manipulation of CD8+ T cell responses may thus provide a unique opportunity to design tumor-specific immunotheraputic approaches, with much less harmful side effects compared to routine radio- and chemotherapies. Saman’s research is focused on natural killer T (NKT) cells, a regulatory cell type capable of quickly producing large amounts of pro- and/or anti-inflammatory cytokines, thus affecting many facets of adaptive immunity, including tumor-specific CD8+ T cell responses. Activation of NKT cells by their glycolipid agonist, typified by α-GalCer, has been the subject of several clinical trials conducted in cancer patients with promising outcomes. However, NKT cell-based therapies are far from optimized. α-GalCer can activate mouse NKT cells in the same way it activates human NKT cells which Provides a good research tool with great potential for benchtop-to-bedside translation. By using α-GalCer and its modified analogs, Saman is trying to activate NKT cells and enhance the magnitude and quality of the CD8+ T cell responses elicited against a well-defined tumor antigen called T Ag in an in vivo mouse model. Saman’s project is expected to help design efficient NKT cell-based therapeutic strategies for cancer and reveal the underlying mechanisms for NKT cell:CD8+ T cell cross-talk in the context of anticancer immunity.
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![]() Rae-Lynn Nesbitt |
Rae-Lynn Nesbitt |
Eldon Ng |
Eldon Ng |
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Teresa Peart Ovarian cancer is the sixth most prevalent cancer in women and is considered to be the most lethal of the gynaecologic malignancies. Early stage disease has a 90% cure rate by surgical intervention alone but over 75% of cases are not diagnosed until advanced metastatic stage. This is mainly due to the fact that early events in ovarian cancer pathogenesis remain to be clearly eluciadated. Thus, there is a critical need to identify etiological factors contributing to ovarian cancer pathogenesis. The goals of our translational ovarian cancer research laboratory are to develop novel research models as tools to study the molecular mechanisms regulating ovarian tumorigenesis with a specific emphasis on bone morphogenetic protein (BMP) signaling. Normal ovarian surface epithelial (OSE) cells as well as epithelial ovarian cancer (EOC) cells possess an autocrine BMP signalling loop. The ID1 and ID3 genes are direct target genes of BMP4 signalling in EOC cells. ID genes are classified as proto-oncogenes because their overexpression in various different cancers can be associated with a less differentiated phenotype and a higher malignant potential, often indicating a poor prognosis. However, little is known of the functional significance of ID1 and ID3 overexpression in ovarian cancer pathogenesis directly. Utilizing various molecular mechanisms to enhance the BMP signalling pathway directly as well as downstream target genes ID1 and ID3, the goal of my project will be to further elucidate the role of BMP signalling pathway in ovarian cancer pathogenesis. |
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Daniela Quail Research Interests: Daniela Quail is a Ph.D. student in the Department of Anatomy and Cell Biology, at the University of Western Ontario, working under the supervision of Dr. Lynne-Marie Postovit. Her research is focused on an embryonic protein called Nodal, which plays a role in promoting stem cell-like characteristics in breast cancer cells. Breast cancer cells that exhibit stem cell-like characteristics tend to be highly aggressive and metastatic. By inhibiting Nodal signalling in breast cancer, she hopes to impede metastatic behaviour. |
Mateusz Rytelewski |
Mateusz Rytelewski |
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Randeep Singh |
Leo Sui |
Leo Sui My research interest involves the development of carbon nanotubes (CNTs) based siRNA delivery system for cancer therapy. It has been reported that CNTs gain into the cells by diffusion and we want to exploit this mechanism for siRNA delivery. siRNA can induce specific gene silencing and which is promising for cancer therapy. However, the stability of siRNA is low and it cannot gain into the cells effectively by itself. We aimed to create a CNTs-based delivery vehicle which can protect the siRNA and deliver the siRNA specifically to cancer cells
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![]() Mike Stewart |
Mike Stewart |
Fartash Vasefi |
Fartash Vasefi |
Ilma Xhaferllari
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Ilma Xhaferllari Respiratory motion is a large source of dosimetric error when treating stage 1 non small cell lung cancer tumours with radiotherapy. When treating patients with Intensity Modulated radiation therapy (IMRT), this motion is susceptible to the interplay effect, which is the independent motion of the multi-leaf collimator (MLC) used to modulate the radiation beam intensity, and the target volume. This is especially important in Stereotactic Body Radiation Therapy (SBRT) where fewer treatment fractions are delivered (<6) compared to conventional techniques (>30), leading to less opportunity of interplay effect to average out over the course of treatment. Respiratory gating, where the beam is only turned on when the patients are in exhalation phase, is one method to reduce the interplay effect. Currently, respiratory gating is only possible with fixed beam and not for Volumetric Modulated Arc Therapy (VMAT) at LRCP. The latest linear accelerator from Varian Medical Systems, TrueBeam, makes gating possible with VMAT. The goal of this research is to determine optimal gating and planning parameters needed for respiratory gated IMRT and to investigate dosimetric effect of respiratory motion on gated IMRT delivery. Respiratory gating has the potential to reduce normal tissue toxicity without compromising tumour coverage. In turn, this will result in potential dose escalation which will improve tumour control and overall survival. |
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Timothy Yeung |
Stephanie Zukowski
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Stephanie Zukowski The prospective project that she will be undertaking encompasses an investigation of the relationship between protein kinase CK2 (formally casein kinase 2) and its involvement in regulating the process of apoptosis in cancer cells. CK2 is a constitutively active serine/threonine protein kinase and the upregulation of CK2 in cancer cells has been shown to promote cancer cell survival by modulating apoptotic machinery. Specifically, apoptotic cysteine-dependent aspartate-directed proteases, known as caspases, are directly regulated by CK2 phosphorylation and secondarily; CK2 phosphorylates downstream targets of caspase cleavage. Notably, evidence has accumulated that CK2 phosphorylation of serine/threonine residues in caspase recognition sites may prevent caspase cleavage required for the progression of apoptosis. The remarkable similarity between the consensus sequence for CK2 phosphorylation and recognition motifs for caspase cleavage suggests that CK2 may play a more prominent role in apoptosis than previously considered. The significance of this discovery invites further research to identify targets of caspase cleavage that are negatively regulated by increased levels of CK2 in cancer cells. This research will elucidate the relationship between CK2 phosphorylation and caspase activity and will then translate the findings to identify cancer cells susceptible to inhibition of CK2.
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Also from this web page:

Navid Baktash
Matthew Cecchini 

Jenny Chu 










Ernie Ho 
Amy Kossert
Lori Lowes 


Teresa Peart
Daniela Quail 



Fartash Vasefi 
Timothy Yeung

