Our People
Awardees

 

 

Mehdi Amiri Malek Hannouf
Navid Baktash Ernie Ho
Matthew Cecchini Michael Jewer
Di Chen Amy Kossert
Choi-Fong Cho Lori Lowes
Jenny Chu Saman Maleki-Vareki
Michael Cohen Rae-Lynn Nesbitt
Rohann Correa Eldon Ng
Courtney Coschi Teresa Peart
Niamh Coughlan Daniela Quail
Alysha Croker Mateusz Rytelewski
Donna Cvetkovic Randeep Singh
Stefanie DeJesus Leo Siu
Christine DiCresce Michael Stewart
Dylan Dieters-Castator Fartash Vasefi
Brandon Disher Ilma Xhaferllari
Stephanie Dorman Timothy Yeung
Vasiliki Economopoulos Stephanie Zukowski
   


 

Medhi Amiri
Medhi Amiri

Mehdi 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 BaktashNavid Baktash

 

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
essential for the metastasis of cancer cells, which accounts for the
majority of cancer mortalities. Investigating the mechanisms leading
to metastatic disease is crucial for the development of novel therapeutics and diagnostics. The goal of our research is to investigate molecular pathways that may be essential for angiogenesis and migratory capacity of invasive prostate and breast cancer cell lines. Identification of targets governing vascular remodelling and tumor migration will yield insights on the development of novel anti- metastatic drugs. Furthermore, such targets can be used as early diagnostic biomarkers predicting metastatic potential, re-occurrence and resistance to chemotherapy. This may significantly contribute to overall patient survival and provide better management techniques for patients with cancer.

 

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Matt CecchiniMatthew Cecchini

 

Matthew Cecchini
has a BSc in Biotechnology from Brock University. He is currently working towards his MD/PhD in Biochemistry under the supervision of Dr. Fred Dick.

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
Di Chen

 

Di Chen
completed her masters training in Immunology in 2008. My current training activities are mainly focused on immunoloy and gene silencing. I started my PhD training under the supervision of Dr. Weiping Min in the Deptartment of Pathology at the University of Western Ontario in January 2009. I will work on the development of anti-cancer therapy through gene-silencing in vivo. I am engaged in basic and translational immune-based anti-tumor therapy (DC vaccines) that have been used clinically since 1996 but with limited success. Although generating new knowledge is an important part of my program, creating better cancer treatments using that knowledge is critical. My research and training program is dedicated to that treatment goal.

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.

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Fong Cho

Choi-Fong Cho

Choi-Fong Cho
is an PhD student in the Department of Medical Biophysics, U.W.O., working under the supervision of Dr. John Lewis. Her project involves studying how non-invasive imaging using nanotechnology should permit detection of early breast cancer before metastasis can occur. Her aim is to construct "smart nanoparticles" that home to the new blood vessels that form around early tumours. She hopes to use these as imaging agents both to diagnose early cancer and to enhance treatment.

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Jenny ChuJenny Chu

 

Jenny Chu
has a BSc in Microbiology from University of Victoria and is currently working towards her MSc in Anatomy and Cell Biology under the supervision of Dr. Alison Allan.
Breast cancer is the number one diagnosed cancer and the number two cause of cancer-related deaths among Canadian women. If detected early, traditional chemotherapy and radiation have a high success rate, but once the disease spreads, or metastasizes, beyond the breast, many conventional treatments fail. A specific type of breast cancer cell, the tumor-initiating cell (TIC), has been proposed to be responsible for primary tumor formation and possibly for tumor spread. My project aims to investigate the interactions between TICs and different organs in the body to determine if these cells prefer one organ over another for secondary metastatic tumor formation. I will use simulated organ environments in culture dishes to assess the effects on breast TIC ability to grow and migrate in different organ environments. By doing so, I hope to further the understanding of the mechanism by which breast cancer spreads and grows in specific organs like the lymph node, brain, lung, liver, and bone. This knowledge could provide new targets for treatment of metastatic breast cancer, which may lead to a reduction of breast cancer related deaths in Canada.

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Michael Cohen
Michael Cohen

Michael Cohen
has an MSc in Microbiology & Immunology from the University of Western Ontario and he is currently working towards a PhD in the same program under the supervision of Dr. Joe Mymryk. Our lab utilizes the Human Adenovirus E1A oncoprotein as a tool to identify novel cellular regulatory proteins and protein interaction motifs regulating eukaryotic cell survival and gene expression, which are highly relevant to many types of cancers. My current research involves characterizing the interaction between E1A and the members of the Dual-Specificity Tyrosine-Regulated Kinase family (DYRK). We hypothesize that the DYRK family of survival kinases mediate oncogenic transformation by adenovirus and human papillomavirus by altering the cellular gene expression of cancer-related DYRK targets involved in cell survival and proliferation.

 


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Rohann Correa

Rohann Correa

Rohann Correa
has a BSc – Honours Biology from the University of Windsor. He is currently working on his MD/PhD at the University of Western Ontario under the supervision of Dr. Gabriel DiMattia and Dr. Trevor Shepherd.

Research Interest:
The goal of our research program is to promote translational ovarian cancer research; specifically, we study the cellular signaling pathways that contribute to epithelial ovarian cancer metastasis. In ovarian cancer, metastasis occurs by exfoliation and diffusion of tumour cells from the primary site followed by establishment of secondary tumours throughout the abdominal cavity.  We model this metastatic process in our laboratory using novel biological systems in order to study cellular signalling in a physiologically relevant context. Of current interest is cellular signalling through the phosphatidylinositol-3-kinase and Akt kinases. These key proteins constitute a ubiquitous growth and survival conduit that can be oncogenic and is often upregulated in ovarian cancer. By examining downstream signalling though this pathway, we aim to characterize cellular mechanisms contributing to epithelial ovarian cancer metastasis. It is hoped that this, in turn, may lead to novel therapeutic strategies to combat advanced stage disease.

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Courtney Coschi

 

Courtney Coschi
completed her BMSc - Honours Specialization in Biochemistry from the University of Western Ontario. She is currently working towards her PhD in the lab of Dr. Fred Dick.

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.

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Niamh Coughlan

Niamh Coughlan

Niamh Coughlan
is a PhD student in the Department of Biochemistry, U.W.O., working under the supervision of Dr. Joseph Torchia. She is studying the p/CIP/CARM1 coactivator complex in estrogen-dependent gene regulation in an attempt to clarify the role of the oncogene p/CIP in estrogen-dependent breast cancers. By identifying key target genes of the complex, and understanding the mechanism that regulates them, the hope is to develop new therapeutic strategies, leading to more effective treatment for p/CIP-overexpressing breast cancers.

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Alysha Croker
Alysha Croker

Alysha Croker
graduated from the University of Western Ontario in 2007 with an Honours BSc in Biology. She is currently working on her PhD in the Department of Anatomy and Cell Biology, supervised by Dr. Alison Allan.

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.

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Donna Cvetkovic

Donna Cvetkovic

Donna Cvetkovic
graduated with a Bachelor of Medical Science Honors Specialization in Physiology from the University of Western Ontario. Currently, she is in her second year of MSc working under the supervision of Dr. Moshmi Bhattacharya, in the Department of Physiology and Pharmacology.

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.

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Stefanie DeJesus

Stefanie De Jesus

Stefanie De Jesus
completed her BSc in Biology and MA in Kinesiology at the University of Western Ontario. She is starting her PhD under the supervision of Dr. Harry Prapavessis at the Exercise and Health Psychology Laboratory, University of Western Ontario. Her research aims to examine cue-elicited cigarette cravings, and the role of acute exercise and nicotine metabolism on smoking behaviour (smoking topography) and withdrawal symptoms.


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Christine DiCresce

Christine DiCresce

Christine DiCresce
completed her undergraduate education at The University of Western Ontario with an Honours BSc in Pharmacology/Toxicology and Psychology and a post-degree minor in Medical Sciences. She is currently a PhD Candidate with the Department of Microbiology and Immunology under the supervision of Dr. Jim Koropatnick.

Antisense molecules targeting TS sensitize human tumour cell lines (in vitro and in vivo) to the effect TS targeting drugs. Her research project explores the possibility that addition of antisense molecules targeting TKs will further sensitize tumour cell lines to the effects of TS targeting chemotherapeutics. She focuses on: (1) using small interfering RNAs (siRNAs) targeting thymidylate synthase (TS) and thymidine kinases (TKs) to enhance the therapeutic effect of anticancer drugs targeting TS, and (2) analysis (including investigation of RISC complex saturation by RNAi and RNAi sequence preferences) of factors affecting the amount of RNAi required to knock down mRNA targets.

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Dylan Dieters-Castador

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.
Research Interests: Nodal is an embryonic protein that regulates cell fate specification and morphogenesis during development. Nodal is normally silenced in adult tissues, but is re-expressed in cancer and is associated with a poor prognosis in melanoma, glioma, prostate cancer and breast cancer. Recent work in our laboratory demonstrated that Nodal is a pivotal regulator of tumour vascularisation in breast cancer, such that it is required for blood vessel recruitment and tumour growth in murine models and is positively correlated with high microvascular density in breast cancer patients. The mechanism by which Nodal regulates tumour vascularisation has not yet been elucidated. Bone Marrow Derived Cells (BMDCs) such as Mesenchymal Stem Cells (MSCs) and Epithelial Progenitor Cells (EPCs) incorporate into growing tumours, and significantly enhance neovascularization. Secretion of cytokines and chemokines into the tumour microevironment has been shown to promote the mobilization and activation of these cell types. However, the mechanisms by which tumour cells acquire the ability to initiate this pro-vasulogenic niche are poorly understood. Given our discovery that Nodal regulates breast cancer vascularisation, as well as the morphogenic role that Nodal plays during embryogenesis, we propose that Nodal mediates BMDC recruitment to breast tumours.

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Brandon Disher
Brandon Disher

Brandon Disher
has a BSc in Physics and High Technology from The University of Windsor. He is currently working on his PhD from The Department of Medical Biophysics, UWO under the supervision of Dr. Jerry J. Battista & Dr. Stewart Gaede.

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.

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Stephanie Dorman

Stephanie Dorman

Stephanie Dorman
has a BMSc Honors Specialization in Medical Sciences and an HBA Honors Business Administration from the University of Western Ontario. She is currently working towards her MSc under the supervision of Dr. Peter Rogan in the Department of Biochemistry.

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.

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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.
Vasiliki is interested in breast cancer metastases to lymph nodes and their early detection, as well as what these events mean for patient prognosis and outcome. Her current project aims to develop and validate a targeted imaging strategy for MRI that will be able to detect micro-metastases.
Vasiliki also currently holds a fellowship award from the Canadian Breast Cancer Foundation – Ontario Region.

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Malek Hannouf
Malek Hannouf

 

Malek Hannouf
has a BSc – Honours in Health Services Management from Philadelphia University. He is currently working on his PhD in epidemiology at the University of Western Ontario under the supervision of Dr. Greg Zaric.
Research Interest:
The goal of our research program is to evaluate genetic tests and genomic applications that are in transition from research to clinical and public health practice; specifically, we evaluate genetic tests that involve tumour gene expression profiling, which promises to be an important tool for the management of patients with cancer (e.g. tumour classification, cancer progression, and chemotherapy resistance and sensitivity). The full impact of these innovations will materialize only when they are effectively and flexibly transferred to clinical practice in cancer patients. We develop decision-analytic models to study the efficacy of new genetic tests and genomic applications in cancer patients and estimate their incremental cost effectiveness versus current clinical practices. Our aim is to characterize the appropriate role of these innovations in actual clinical practice. It is hoped that this, in turn may move new cancer diagnostics and therapeutics faster and more cost effectively from bench to bedside; and ultimately to realize the potential of personalized medicine to improve cancer patient outcomes such as survival.

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Ernie HoErnie Ho

 

Ernie Ho
has a BSc (Hons) in Marine and Environmental Biology from The Hong Kong University of Science and Technology. He is currently working on his PhD in Physiology and PhD in the Collaborative Program in Developmental Biology under the supervision of Dr. Lina Dagnino.

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
Michael Jewer

 

Michael Jewer
attained his B.Sc Honours Biology with a specialization in Molecular Biology and Biotechnology at the University of Waterloo.

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 KossertAmy Kossert

 

Amy Kossert
is a 4th year PhD student under the supervision of Dr. Harry Prapavessis at the Exercise and Health Psychology Laboratory, University of Western Ontario.

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 LowesLori Lowes

 

Lori Lowes
has a BMSc in Microbiology and Immunology from the University of Western Ontario. She is currently working on a PhD in Anatomy and Cell Biology in Dr. Alison Allan's lab.

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.
In collaboration with Dr. Tracy Sexton, the CSS will be used to investigate the role of CTCs in prostate cancer patients who need radiation for a rising PSA level post surgery. First, we will look at blood samples of patients (n=20) prior to and 3 months after radiation in a pilot study, assessing the numbers of CTCs present. If CTCs are detected and those numbers change after treatment then we will move to a larger follow-up study which will involve the collection and analysis of multiple blood samples for CTCs over a 2 year period. These numbers will then be correlated with the success of radiation and overall survival.

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Saman Maleki-Vareki
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

Rae-Lynn Nesbitt
completed a Hons. BSc in Biology from the University of Western Ontario, 2009. Currently a PhD Student in the Department of Medical Biophysics, under the supervision of Dr. John Lewis.

Prostate cancer is the most common cancer in Canadian men. Most chemotherapeutic drugs do not preferentially target the tumour and therefore subject the patient’s healthy cells to significant toxicity. The reptilian reovirus-derived FAST protein p14 endogenously mediates rapid cell-cell fusion. When p14 is incorporated into liposomes, it significantly increases the fusion of liposomes to cell membranes, bypassing the degradative endocytic pathway. The p14 protein can accommodate  the incorporation of targeting peptides so that liposomes with both cell-specific and fusogenic properties may be conferred by a recombinant p14. Previous research in our lab has verified bombesin as an effective targeting peptide for gastrin releasing peptide (GRP) receptors, which are up-regulated in many human tumours including prostate cancer. I am using this fusogenic liposome platform to target a toxic therapeutic payload to prostate tumours. This therapeutic strategy could effectively lower the overall dose needed to achieve a reduction in tumour burden while minimizing harmful side effects.

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Eldon Ng

Eldon Ng

Eldon Ng
is an MSc student in the Department of Medical Biophysics working under the supervision of Dr. Jeffrey Carson. Eldon is working on developing a novel hybrid optical imaging system that combines the high contrast of optical imaging methods with the resolution of ultrasound detection. The hybrid Angular domain and Photoacoustic imaging system will be used to image surgically resected breast tissue samples and detect the presence of cancerous cells near the tissue margins

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Teresa PeartTeresa Peart

 

Teresa Peart
holds a BSc Honours Specialization in Cell and Developmental Biology, fromt the University of Western Ontario. She is currently working towards a PhD in Anatomy and Cell Biology, and is supervised by Drs. Trevor Shepherd and Gabriel DiMattia (Translational Ovarian Cancer Research Program).

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 QuailDaniela Quail

 

 

Daniela Quail
has a B.Sc. in Biology from the University of Western Ontario, and is currently a Ph.D. candidate under the supervision of Dr. Lynne-Marie Postovit.

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.

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Mateusz Rytelewski

Mateusz Rytelewski

Mateusz Rytelewski
is a PhD student in the Department of Microbiology and Immunology, under the supervision of Dr. Koropatnick. His research is focused on targeting DNA repair enzymes using antisense strategies, in combination with anti thymidylate synthase (TS) treatment, to investigate the effects of this therapeutic regimen on human tumour cell survival and growth. Though reduced DNA repair capacity caused by mutations in DNA repair enzymes and transcription factors increases patient susceptibility to disease, clinical data suggests that the presence of these same mutations in cancer cells increases the success of cancer therapy. He will also be exploring the mechanistic details which modulate cancer cell biology in this system, including the possible contribution of the immune system

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Randeep Singh
Randeep Singh

 

Randeep Singh
holds a BMSc. (Honors Biochemistry), and a MSc. (Biochemistry) from the University of Western Ontario. She is currently working on her PhD in Developmental Biology under the supervision of Dr. Lina Dagnino.

During development, E2F1 functions as a central hub to determine cell’s fate to either proliferate or differentiate. Many cancer cells use the proliferative advantage given by E2F1. Post-translational modifications of E2F1 regulate its turnover, which is required for differentiation. In many cancer cells, the pathway leading to E2F1 degradation appears to be impaired. Therefore, I hypothesize that post-translational modifications including ubiquitination and/or phosphorylation promote E2F1 turnover and differentiation, inhibiting carcinogenic transformation.   The purpose of my studies is to elucidate the mechanisms leading to E2F1 degradation, thus identifying key players which could serve as potential targets for therapy.

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Leo Siu

Leo Sui

Leo Sui
graduated his Mphil in The University of Hong Kong. He is currently a second year PhD student under the supervision of Dr. Weiping Min in Department of Pathology, University of Western Ontario.

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

Mike Stewart
has a B.M.Sc. and honors in Physiology and Pharmacology from the University of Western Ontario. He is currently a 1st year PhD student in Physiology under the supervision of Dr. Dale W. Laird.

Decreased connexin levels have been observed in a wide variety of cancers, including breast cancer. As a result, connexins have been proposed to act as tumour suppressors but their role in breast cancer onset, progression and metastasis remains poorly understood. Similarly, pannexins were recently identified to be differentially regulated in the mammary gland and have single membrane channel function not unlike connexin hemichannels.  Importantly, pannexins have been shown to have tumor suppressive properties in gliomas but their role in the mammary gland development, differentiation and tumorigenesis is completely unknown. It is our aim to further our understanding of the role connexins and pannexins in mammary gland differentiation and tumorigenesis.

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Fartash VasefiFartash Vasefi

Fartash Vasefi
Dr. Fartash Vasefi is a Postdoctoral Associate in the Department of
Medical Biophysics, U.W.O. and the Lawson Health Research Institute,
working under the supervision of Dr. Jeffery J. L. Carson. His
research is focusing on the development and evaluation of a novel
spectroscopic imaging technology to assist in characterization and
high resolution margin delineation of cancerous tissue during surgery.
Fartash hopes the new technology will enable physicians to
differentiate between normal and malignant tissue based on their
specific optical abnormalities.

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Ilma Xhaferllari

Ilma Xhaferllari

 

Ilma Xhaferllari
completed her B.Sc. in Physics and High Technology through the University of Windsor. She is currently working towards her M.Sc. degree through the department of Medical Biophysics under the supervision of Dr. Stewart Gaede.

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 YeungTimothy Yeung

 

Timothy Yeung
graduated from the Radiation Therapy Program that is jointly offered by the University of Toronto and The Michener Institute for Applied Health Sciences. He is currently a PhD student in the Department of Medical Biophysics and working under the supervision of Drs. Slav Yartsev and Glenn Bauman. He also collaborates closely with Dr. Ting-Yim Lee.

His research investigates the application of dynamic contrast-enhanced computed tomography (DCE-CT) and positron emission tomography (PET) in brain cancer radiation herapy. We aim to identify biologically significant tumour sub-volumes based on imaging of brain tumour metabolism (using positron emission tomography, PET), tumour perfusion (using dynamic contrast-enhanced CT, DCE-CT), and tumour hypoxia (PET + DCE-CT) by correlating the volumes with sites of eventual tumour relapse in the brain after conventional radiation therapy. By doing so, we hope to gain insight as to whether functional imaging (PET and/or DCE-CT) can provide clinically important information that could improve radiation treatment for patients with malignant glioma.

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Stephanie Zukowski

Stephanie Zukowski

 

Stephanie Zukowski
has a BMSc Honors Specialization in Biochemistry and Cell Biology from The University of Western Ontario and is currently working towards her MSc in Biochemistry under the supervision of Dr. David W. Litchfield.

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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