CIHR – Porter Lab

UNDERGRADS 2026

fidalgo — Wed, 13 May 2026 13:48:44 +0000

Glioblastoma (GBM) is the most common and lethal primary malignant brain cancer. Despite standard treatments, the average life expectancy is only about 15 months, and majority of patients experience recurrence of this aggressive cancer within a couple years of their initial diagnosis. A major obstacle that prevents successful treatment of GBM is the presence of glioma stem cells (GSCs), a small group of tumour cells that can evade standard of care treatment and regrow the tumour. This challenge is aggravated by components of the tumour microenvironment, including endothelial cells (ECs), that may enhance the maintenance of GSCs through the secretion of critical factors and direct cell-cell contact interactions. The complexity of this interaction is further heightened by the presence of notable GSC cell-surface markers, CD44 and CD133, which can be present alone or in combination as different subpopulations of GSCs. These GSC subpopulations can potentially interact with ECs in different ways to promote GBM aggressiveness. My research focuses on exploring this intricate interaction using patient-derived GSCs, graciously provided by Windsor Regional Hospital and Henry Ford Hospital, along with endothelial cells in in vitro experiments. We also utilize an in vivo fluorescent zebrafish model that allows us to study the interaction between the vasculature and patient-derived GSC subpopulations.

My journey in Porter Lab has been one of the most transformative and rewarding experiences of my undergraduate career. During my first year in lab, I built a foundational understanding of cancer cell biology and was exposed to its applications through shadowing upper-year researchers and participating in the Peer Mentoring Network. Over the years, I developed key skills in lab technique, critical thinking, and collaboration, which proved instrumental when I was given the privilege of having my own research project. From my very first moment in lab, I have been supported by a team of talented researchers that have fostered my personal growth and deepened my appreciation for the intricacies of cancer research. I am extremely grateful for the precious mentorship, support, and opportunities that Dr. Porter, Dr. Lubanska, and the entire Porter Lab team have provided me. This journey has inspired me to continue contributing to scientific discovery and the broader fight against cancer!

My project studies neuroblastoma, a cancer arising from the nervous system, and the most common extracranial tumour in children. A challenge when treating high-risk neuroblastoma is “intra-tumoral heterogeneity”, or the idea that one tumour can be comprised of sub-populations of different cell types, each with unique characteristics and markers. This nature of neuroblastoma makes targeted therapies somewhat ineffective, and thus, my project looks towards an efficient and effective way to analyze protein activity within a neuroblastoma model on a cell-by-cell basis. Through a collaboration with the Department of Computer Science, I have optimized and utilized a high-throughput bioinformatics tool called “ICCell” to help us determine abundance, localization, and activity of various proteins using fluorescent microscopy. This tool not only helps advance knowledge on neuroblastoma, revealing potential targets for treatment, but can be applied across multiple disciplines in biomedical sciences or various general science research fields.

My time in the Porter Lab over the past three years has been nothing short of highly motivating and rewarding. I have grown close to so many mentors and friends throughout this journey, all of which have shaped who I am as both a researcher and a person. Further, the opportunities I have had to expand my research, namely through the Brain Tumour Foundation of Canada Summer Studentship, have not only helped advance my knowledge, but more importantly, connected me with a community of individuals who share the same passion for this field of healthcare. I am beyond grateful for all the guidance I’ve received from Dr. Porter, Dr. Lubanska, and the entire Porter Lab team; this experience has solidified my passion and interest for pursuing a future career to help advance cancer research.

Tuberous Sclerosis Complex (TSC) is a rare genetic disorder caused by mutations in the TSC1 and TSC2 genes, which encode the proteins Hamartin and Tuberin. Together, these proteins regulate cell growth, nutrient-responsive signaling, and tumor suppression. As a result, TSC is associated with abnormal cell division and tumour formation in multiple organs, including the brain, kidneys, lungs, and skin. Our lab studies Tuberin and its role in cell cycle regulation, where it binds cyclin B1 and delays mitotic onset, allowing cells more time to grow and prepare for division. Previous BioID proximity-labeling studies performed in our lab identified LAMTOR1, a lysosomal scaffold protein involved in nutrient sensing, as the only protein to co-enrich with Tuberin, Hamartin, and CDK1 under stringent criteria. My project investigates the relationship between Tuberin and LAMTOR1 through localization and interaction studies to better understand whether these proteins may contribute to a mechanism linking nutrient sensing with cell cycle regulation.

My journey in Porter Lab has been one of the most rewarding experiences of my undergraduate career, and I have grown tremendously both scientifically and personally since joining the lab. Through the Peer Mentor Network, I had the opportunity to learn about the research projects of thesis students while I was still a pre-project student, which further strengthened my interest in research and allowed me to learn from students I looked up to as role models. I also had the opportunity to shadow students in the lab, develop new technical and critical thinking skills, and gradually grow more confident in my own abilities as a researcher. Over the past year, I have been able to present my research and further develop my communication and problem-solving skills while gaining a much deeper appreciation for the complexity of scientific discovery. I am extremely grateful for the mentorship and support I have received from Dr. Porter, Dr. Fidalgo Da Silva, and the entire Porter Lab team, whose guidance and encouragement have made my undergraduate research experience incredibly meaningful. The experiences and skills I have gained in Porter Lab will continue to support me throughout my future in science and research.

UNDERGRADS 2025

fidalgo — Wed, 14 May 2025 14:53:46 +0000

Christopher Jaworski

Glioblastoma (GBM) stands as one of the most lethal and aggressive brain cancers, often defying current treatment strategies. The outlook for patients remains grim, with average survival hovering around just 14 months after diagnosis. A major reason for this is the tumor’s ability to resist therapy and recur, often driven by a complex network of cellular interactions within the tumor microenvironment. My research focuses on understanding the relationship between glioblastoma and a group of cells known as cancer-associated fibroblasts (CAFs). CAFs play a critical role in shaping the tumor environment by promoting tumor growth, supporting resistance to therapies, and enhancing invasive behavior. A protein of particular interest in our studies is YKL-40—a glycoprotein that is highly expressed in the mesenchymal subtype of GBM. This subtype is known for its aggressive nature and poor response to conventional treatments. By investigating how CAFs and tumor-initiating cells communicate through YKL-40, we aim to identify vulnerabilities that could lead to more effective treatment strategies. We’re also working with brain tumor organoids to model these interactions more realistically, and using techniques like shRNA knockdowns to probe the role of YKL-40 more precisely.

My journey in research began in my second year of university when I joined the Porter Lab. I entered as a volunteer, initially gaining exposure to the fundamentals of cancer biology. Through the Peer Mentor Network, I was mentored by upper-year students who helped me develop a foundational understanding of lab techniques and experimental design. As I grew more confident and capable, I began contributing more directly to ongoing experiments and even helped identify gaps in existing research that informed new directions for study. By the time I reached my upper years, I had the privilege of having my own project, from hypothesis formation to troubleshooting complex protocols. This experience has sharpened my analytical thinking and strengthened my collaborative skills, especially through interdisciplinary discussions with researchers across different fields. Being part of such a dynamic lab has deepened my appreciation for the intricacies of cancer research and sparked a commitment to lifelong learning and scientific inquiry. I’m incredibly thankful to Dr. Porter and the entire lab team for their mentorship, support, and trust in my development. This journey has not only shaped my academic path but also inspired me to continue contributing to the broader fight against cancer.

Glioblastoma (GBM) is the most aggressive type of brain tumour, characterized by its highly infiltrative and heterogeneous nature, which poses significant challenges to standard therapies. The presence of therapy-resistant Glioma Stem Cells (GSCs) contributes to GBM heterogeneity. Cancer cells (including GBM) are characterized by uncontrolled cell proliferation, which is linked to cell cycle dysregulation. SPY1 (SPDYA/RingoA) is an atypical cell cycle regulator that overrides cell cycle checkpoints, aiding in uncontrolled cell proliferation and survival through unique activation of CDKs. In GBM, elevated levels of SPY1 regulate CDK2 activity and drive clonal expansion of CD133+ GSCs. SPY1-CDK2 can also activate RNA-binding protein, Musashi-1 (MSI1), which plays a critical role in GSC maintenance through post-transcriptional regulation of NUMB and Notch pathway. MSI1 supports GSC populations to drive tumor

initiation and resistance to differentiation. This study aims to understand the role of MSI1 in maintaining GSC properties and its potential correlation with specific subgroups, and how MSI1 influences GSC self-renewal, proliferation, and response to therapies, with the goal of identifying novel therapeutic strategies to overcome treatment resistance in GBM. To demonstrate this, established GBM cell lines were infected with short hairpin (sh) MSI1 lentivirus, which resulted in reduced proliferation and self-renewal. The Zebrafish PDX platform was used to further validate the effects, confirming the impact of the MSI1 knockdown

Being part of the Porter Lab family was one of the most amazing and rewarding experiences of my undergraduate studies. It offered far more than experimental training – it provided a supportive, intellectually stimulating environment where I learned to think critically, troubleshoot experiments, and develop my intrapersonal skills, which will help me in the real world. From the beginning, I was welcomed into a community that values both scientific excellence and personal growth. Whether it was executing the experiment, analyzing data, or collaborating with your lab peers, every task contributed to my development as a researcher. The most important thing I’ve learned during the whole experience is the value of perseverance. You are bound to experimental errors that may alter your results, but you have to see these setbacks as opportunities to rethink and improve, not as failures.

Glioblastoma (GBM) is the most lethal and aggressive primary brain tumour affecting the central nervous system. Despite standard treatments, prognosis remains poor due to several barriers that limit successful treatment such as the presence of the blood-brain barrier, tumour heterogeneity, and glioma stem cells (GSCs). GSCs are known to increase aggressiveness and hinder therapy response. A notable GSC marker is the CD44 receptor, which is activated by its primary ligand, hyaluronic acid (HA), to promote cancer progression. High CD44 expression in GBM is correlated to increased aggressiveness, stemness, proliferation and, ultimately, poorer prognosis. Nanoparticle therapies are an emerging field of cancer research that allow for selective targeting of GSC populations. Our lab has shown that HA-Conjugated Nanoparticles (HA-CPNs) can selectively target CD44+ cells, eliciting anti-tumour effects both in vitro and in vivo. Within my project, I utilize HA-CPNs to target GSC populations within a biologically relevant model known as glioblastoma organoids. Organoids mimic real 3D tumour tissues making them a suitable model to study the effects of HA-CPNs on GSC regulation.

My journey within Porter Lab, starting in my second year of undergraduate studies, has provided me with some of the most rewarding experiences of my entire undergraduate career. I have been extremely fortunate to work alongside a team of talented students and RAs that I view as incredible role models and mentors. My time in lab has expanded my ability to problem solve, think critically, and above all has made me a more resilient person, appreciative of the intricacies of scientific discovery. I am extremely grateful for all of the opportunities, support, and guidance I have received from Dr. Porter, Dr. Lubanska, and the whole Porter Lab team this past year!

My project focuses on determining the potential of the CDK1/2 inhibitor Dinaciclib as a therapeutic direction for prostate cancer (PC). Adenocarcinoma prostate cancer (AdPC) represents 95% of all PC cases and has several treatment options available, such as surgery, chemotherapy, and hormone therapy, like androgen deprivation therapy (ADT). ADT works by blocking the production of androgens in the body, such as testosterone, to reduce the proliferation of prostate cancer cells. However, some patients do become resistant to ADT, leading to treatment-resistant populations of PC to emerge, called castration-resistant prostate cancer (CRPC). CRPC has a median-survival rate of 1-2 years and is much more aggressive than AdPC. A common treatment method used for CRPC is AR inhibitors, which block the activity of the androgen receptor (AR) outright to slow the proliferation of the prostate cancer cells. However, patients can also become resistant to this form of therapy, and differentiate into a treatment-resistant form called neuroendocrine prostate cancer (NEPC). NEPC is the most aggressive and deadly subtype of prostate cancer, and has a 7-month median survival rate. Furthermore, the downregulation of prostate-specific membrane antigen (PSMA), an important detection target, and AR in the transdifferentiation to NEPC further contribute to the poor prognosis of this type of cancer. Our lab proposes targeting the cell cycle to slow the proliferation of prostate cancer, using a CDK1/2 inhibitor named Dinaciclib. My project uses three prostate cancer cell lines to test the efficacy of Dinaciclib in vitro in stopping the proliferation of prostate cancer cells: LNCaP-FBS, an AdPC cell line, LNCaP-CSS, a CRPC cell line, and NCI-H660, an NEPC cell line. My project also uses zebrafish as an in vivo model to test Dinaciclib’s effect on tumour burden, where zebrafish have been injected with prostate cancer cell lines and treated with Dinaciclib. Zebrafish are a viable model for prostate cancer because they develop rapidly, have transparent embryos, which makes them easy to see under a microscope, and also lack an immune system within their first 10 days of life, decreasing the chance of rejection if they were to be given human cells.

My time in Porter Lab has been one of the most important and fulfilling experiences of my life because it has allowed me to grow not only as a scientist but also as a learner. I would like to express my sincere gratitude to my supervisors Dr. Lisa Porter and Dr. Elizabeth Fidalgo da Silva, as well as PhD and master’s students for their mentorship, encouragement, and guidance in developing my research ability. I wish the best of luck to the next group of thesis undergraduates!

Undergrads – 2023

fidalgo — Thu, 04 May 2023 18:47:44 +0000

Amy Llancari

My project focuses on differentiating the progression of Non-alcoholic Fatty Liver Disease (NALFD) into Hepatocellular Carcinoma (HCC) between male and female mice. HCC is the sixth most prevalent cancer in the world, yet it ranks as the third leading type of cancer deaths with an accelerated increase in incidence rates. NAFLD is a major risk factor for HCC, and is emerging as the most common chronic liver condition in the Western world. Prevalence of both HCC and NAFLD is significantly higher in men than women worldwide, suggesting sex-specific differences may play a role in disease susceptibility. My project will focus on investigating these sex-specific morphological and cell expression pattern differences. This will provide insight on potential protective mechanisms found in female mice inhibiting liver injury, in addition to potential diagnostic markers and molecular treatment targets during NAFLD progression.

I have been part of the Porter since my first year of undergrad. My time in the Porter Lab has been the highlight of my university career. I cannot put into words how thankful I am for the unwavering support and guidance I’ve received throughout my project. Dr. Porter and the RA’s have been exceptional role models, their dedication to the scientific community is truly inspiring, and their passion for research is contagious. Being a part of this incredible team has been an honor, and has provided me with so many opportunities both in research and community involvement. My time in the lab has taught me valuable research skills, as well as transferable skills that I will carry with me throughout my career. As I pursue my Masters in the Porter Lab, I am excited to continue to learn and grow as a researcher.

Alan Cieslukowski

Efficient targeting of multiple components of a tumour might be a successful strategy in aggressive types of cancer such as glioblastoma (GBM), which remains the most common and malignant primary brain tumour with an extremely poor patient survival of less than 15 months. The significant therapeutic challenge posed by GBM stems from its genetic and phenotypic heterogeneity fueled by characteristics such as aggressive and treatment-resistant populations of Tumour Initiating Cells (TICs) and high levels of angiogenesis contributing to tumour evolution. TICs, which are responsible for GBM patient relapse, thrive in niches close to blood vessels where they interact with endothelial cells (ECs), exit the cell cycle, and evade therapies. Targeted antiangiogenic drugs, preventing GBM cells from recruiting new blood vessels are only temporarily effective in 50% of patients, resulting in acquired secondary resistance by the tumour. This project explores the TIC-EC interplay and its role in propagating tumour aggressiveness and therapy resistance. This project investigates the impact of ECs on the aggressive characteristics of individual, specific populations of TICs using GBM patient-derived systems, including 3D organoid models and zebrafish patient-derived xenografts (PDXs). Considering that NOTCH1 signaling regulates both TIC and EC populations in GBM, this project dissects the role of NOTCH pathway in TIC-EC interaction. Elucidating the details of cell cycle signaling and specific populations of aggressive TICs with dependence on the EC component will contribute to the identification of new and better therapeutic targets and personalized approaches to treatment of patients with GBM in the future.

Depen Sharma

Tuberous Sclerosis Complex (TSC) is a genetic disorder affecting 1 in 6,000 births, leading to benign tumour formation in various body parts such as the brain, kidney, skin, and lungs. This condition arises from mutations in the TSC1 or TSC2 genes and presents a wide range of neurological symptoms, making diagnosis challenging. Tuberin, a protein encoded by the TSC2 gene, is critical in regulating cell growth, proliferation, and the cell cycle. A key element in TSC is the interaction between Tuberin and Hamartin, encoded by the TSC1 gene. Hamartin ensures Tuberin stability by inhibiting its interaction with the E3-ligase HERC1, which would otherwise lead to Tuberin degradation. Tuberin also regulates the G1/S and G2/M checkpoints in the cell cycle, which are crucial for controlling cell growth and division.

Our research explores the potential role of Cyclin B1, a cell cycle protein, in stabilizing Tuberin levels without Hamartin. Cyclin B1 is essential for mitotic entry, and its function has yet to be entirely understood. It has five serine residues that can be mutated to create a phospho-null Cyclin B1 construct (Cyclin B1 5A), which we utilize in our investigation. Previous work has shown that Tuberin can bind Cyclin B1 during the G2 phase of the cell cycle, but more is needed to know about their interactions when Hamartin is present. Cyclin B1 may be essential in Tuberin stabilization during the G2/M transition. Understanding the relationship between Cyclin B1 and Tuberin in TSC could provide valuable insights into the disorder’s molecular mechanisms and potentially lead to novel therapeutic approaches. By elucidating the role of Cyclin B1 in Tuberin stabilization, we hope to contribute to the ongoing efforts in understanding and treating Tuberous Sclerosis Complex.

Emmanuel Boujeke

My research focuses on Glioblastoma (GBM). GBM is the most frequent and aggressive primary brain tumour in adults. GBM patients have an extremely poor prognosis, with survival averaging only 14 months post-diagnosis. Our lab has been investigating the role of a novel cell cycle regulator (Spy1) in the development and progression of many cancers, including GBM. The focus of my project is to investigate the interplay between Spy1 and some of the known drivers of GBM. Using a transgenic mouse model created by the lab, I study the impact of Spy1-mediated effects on gene expression, self-renewal potential, stemness, and oncogenic transformation in the face of aberration in selected oncogenes and tumour suppressors known to drive glioma progression in neural stem cells.

I joined the Porter Lab at the beginning of my second year of University as an outstanding scholar. Having no prior research experience, I felt intimidated and unsure, worried that I would not be good enough for the lab. Fast forward to two years later, I can now say that joining the Porter Lab was one of the best decisions I made in university. Being surrounded by intelligent, motivated, and driven people inspired me to be persistent and hardworking both inside and outside of the lab. Through my thesis, I learned to think critically and creatively, mentor others, and overcome obstacles. The RA’s and Dr. Porter were exceptional role models and provided unconditional support despite my frequent mistakes. Through this experience, I learned what it means to do research and found my place in it.

Lia Oschanney

Liver cancer is one of the leading causes of cancer death globally, of which 90% of cases are Hepatocellular Carcinoma (HCC). One risk factor of HCC is Non-Alcoholic Fatty Liver Disease (NAFLD), often triggered by sedentary lifestyle, poor diet, and obesity. Most cases of HCC are cirrhotic and can start from excess fat accumulation in NAFLD. Chronic fat can trigger inflammatory responses that damage cells, leading to the liver initiating a proliferative response to recover. However, over time the liver shifts to a fibrotic state to maintain structural integrity with low levels of proliferation, characteristic of Non-Alcoholic Steatohepatitis (NASH). As fibrosis becomes extensive, the liver becomes cirrhotic, and the environment increases HCC risk; however, 20% of HCC cases are non-cirrhotic arising directly from NAFLD. The atypical cyclin-like protein Spy1 is capable of binding to CDKs, increasing cell division and overriding checkpoints. Spy1 has been shown to have a role in cancers, including HCC. Previous research has shown that mice with an overexpression of Spy1 in the liver develop NAFLD and HCC with decreased fibrosis, suggesting that elevation of Spy1 drives a proliferative response in the presence of cell damage, thus increasing HCC risk. To better understand the mechanisms that govern this response and the role of Spy1, this project examines NAFLD development in a transgenic mouse model driving Spy1 overexpression in the liver. This work may lead to the use of Spy1 as a potential drug target in the treatment of HCC.

In my first year, I knew I had a strong interest in research, but I was unsure how to take the first steps towards getting involved. Then, I discovered Dr. Porter’s website and was immediately captivated by the amazing work being conducted in the lab. However, just as I was eager to get started, the pandemic hit, and I was unable to set foot in the lab for nearly two years. Despite this obstacle, the lab kept me engaged through peer mentoring, which continued to fuel my curiosity and teach me the fundamental principles underlying research. When I finally had the opportunity to work in the lab as a third-year student, I had limited practical experience due to the majority of my undergraduate studies occurring online. However, under the guidance of the Porter lab team, I learned a multitude of techniques and quickly progressed from a hesitant and uncertain beginner to a confident and independent researcher capable of working on my own project. This experience has not only prepared me for future research endeavors but has also equipped me with invaluable skills that will undoubtedly serve me well in my future career in medicine. Completing my undergraduate thesis was an incredibly rewarding experience, and it would not have been possible without the support of my peers and the guidance of Dr. Bre-Anne Fifield and Dr. Lisa Porter. I am grateful for the opportunity to have worked in such an inspiring environment and to have learned from some of the brightest minds in the field.

Vanessa Vuong

The cell cycle contains checkpoints that delay mitotic progression and allow for DNA repair before cell division. Our cells receive thousands of DNA lesions a day and this damage can be caused by radiation, drugs, and other processes, leading to cellular mutations and carcinogenesis. There are two types of damage, single-stranded DNA breaks or the more lethal double-stranded DNA breaks (DSB). Upon receiving DSBs, the DNA damage response (DDR) pathway activates p53, which is a tumour suppressor protein that induces apoptosis or cell cycle arrest for cellular repair. Tuberin (encoded by the TSC2 gene) is another tumour suppressor protein that regulates the G2/M transition in the cell cycle and negatively regulates protein synthesis and cell growth. Mutations in tuberin can lead to the multisystem autosomal dominant disease known as tuberous sclerosis (TSC). Porter lab has previously shown that regulates mitotic onset through cellular localization of the G2/M Cyclin, Cyclin B1. My project focuses on the Tuberin/Cyclin B1 complex and its role in G2/M arrest for DNA damage repair. In this study, tuberin knockout NIH3T3 (mouse) cells were created using CRISPR editing technology. The cells will then be treated with etoposide, which is a chemotherapy agent that forms a complex with DNA and topoisomerase II to prevent DNA religation and this induces DNA damage. Wildtype NIH3T3 cells are compared to the knockout line and their cell cycle profile and DNA damage will be visualized using flow cytometry. Results have shown that without the prescence of tuberin, cells will return to G1 much faster since tuberin is not present to bind to cyclin B1 to prolong G2/M arrest. This project will provide greater insight into DNA damage induced carcinogenesis, TSC, and other proliferative diseases.

Joining Porter lab as a member of the peer mentor network and eveutally moving up to complete my undergraduate thesis was truly the best experience! I got to meet many wonderful people who help guide me throughout my struggles with getting data, especially those in the tuberin group who I had to see everyday. The problem-solving, critical thinking, and hands-on techniques I learned during my thesis are skills that I will certainly use in my future career. Best of luck to the incoming thesis students and new undergrads!

Undergrads 2022 – part 1

fidalgo — Mon, 09 May 2022 23:16:25 +0000

Control of Stemness in Glioma via Nanoparticle-Mediated Regulation of CD44 Receptor

Glioblastoma, also known as glioma or GBM, is the most common and aggressive malignant primary brain tumor which continues to puzzle researchers as decades of efforts to find an effective therapy has proven to fail. Barriers to success of the available treatment include impermeability of the blood brain barrier (BBB) to drugs, tumor heterogeneity, and existence of aggressive and resistant Tumour Initiating Cells (TICs). Collaborative studies in our lab show that conjugated polymer nanoparticles (CPNs) can serve as a potential therapeutic approach to overcome these barriers. CPNs are labeled with hyaluronic acid (HA-CPNs) which is a ligand for one of the most prominent receptors found on TICs, CD44. Our data to date has demonstrated that HA-CPNs cause selective decrease in proliferation, migration potential, and expression of markers of aggressiveness and self renewal in CD44+ glioma cells. This study investigates the mechanism by which HA-CPNs exert their effects and how the uptake of the nanoparticles is regulated. We study the status of CD44 receptor on the protein and mRNA levels as well as how manipulation of its levels affects glioma aggressiveness. We explore inhibition of Clathrin Mediated Endocytosis as responsible for the uptake of HA-CPNs and use it to validate selected effects of HA-CPNs. This work will reveal molecular mechanism behind HA-CPN anti-glioma effects which will further contribute to more in- depth evaluation of this nanoparticle system as a potential therapy for patients with GBM.

“Since joining Porter Lab in my second year of undergrad, I would have never thought this experience would have been so rewarding. Before my time in the lab, I had little knowledge of what the research side of academia was like. Through the COVID-19 pandemic, I found myself thinking largely about my future and through working in the lab via virtual platforms and maintaining my interest in research, I began my thesis in my forth year in person. Although this experience was such a learning curve, I have never been so appreciative and lucky to have this opportunity. Learning and gaining valuable skills in the lab such as trouble-shooting, team work, and resiliency, I can honestly say research has become such a passion of mine.

In my time in Porter Lab, I have created so many friendships with my fellow lab mates that I know will last forever. If you asked me in my first year what I thought I would accomplish during my undergrad, I would have never thought I could say that on a micro level, I am contributing to the advancement of cancer research in my community. I am excited to pursue my masters degree in biological sciences with Porter lab and eager to see all the change each and every member contributes to cancer research.”

Novel Cell Cycle Therapeutic Strategy Against Type II Medulloblastoma

Medulloblastoma (MB) is one of the most common malignant brain tumours, occurring mainly in children between the ages of 1 to 9 years. The standard of care which is currently being applied for MB includes combination of radiation, surgery, and chemotherapy. This treatment is aggressive and is only effective for a small percentage of patients due to the presence of aggressive and therapy resistant populations of Tumour Initiating Cells (TICs). A recent approach in clinical trials is the use of cell cycle regulator proteins, CKIs, which are synthetic cyclin-dependent kinase inhibitors. Our lab focuses on a specific cell cycle regulatory protein, Speedy (Spy1) which promotes proliferation and overrides cell cycle checkpoints established by natural CKIs. Spy1 plays a role in the maintenance and expansion of stemlike populations of TICs in different types of brain tumour. It is our hypothesis that Spy1 can drive tumour initiating cells in medulloblastoma in face and despite ongoing therapy. In this study we investigate and reveal the role of Spy1 in MB in response to known therapeutic agents and Spy1 mediated effects on the dangerous TIC populations in the treatment setting. In addition, Sonic hedgehog (Shh) MB, a type 2 medulloblastoma, is studied and manipulated to assess potential effects of Shh pathway in the regulation of Spy1. This project is the first one to demonstrate that standard of care treatment of MB leads to increased levels of Spy1 and selection of resistant TIC populations. We show that a key molecular driver in MB plays a role in the regulation of Spy1 levels which is an important finding in further studies seeking for novel effective therapeutic strategies against MB. Overall, my project will contribute to better understanding of the role of Spy1 in MB and its application as a potential therapeutical target in the future.

“Joining the Porter Lab at the end of my first year was the best decision I made in my University experience; it was life changing. I met a lot of amazing, professional and talented people that I am proud to call them my family now. I gained a lot of unique skills like patience, problem solving and critical thinking in addition to a lot of new techniques. I learned to never give up and most importantly passion in cancer research as without hope there is no meaningful research. My work in the lab was affected by Covid-19 but with the help of Dr. Porter, the RAs, the grad students and the mentor network I was able to overcome many challenges. We are a true family that stands which each other. Joining the Porter Lab helped me better understand the importance of cancer research and value the importance of hard work. My experience in the lab helped realize that I want to pursue a career that involves research in the future. I learned something new every minute I spent in the lab and this experience increases my desire in continuing to learn more and more every day. I am very grateful for my experience in the Porter Lab and I am proud to call myself a Porter Lab rat.”

The Role of Tuberin in DNA Damage Repair During Cell Proliferation

The cell cycle contains DNA damage checkpoints that delay mitotic progression and allow for DNA repair before cell division. DNA damage can be caused by radiation, drugs, and other processes which lead to cellular mutations and carcinogenesis. The tumour suppressor protein p53 is activated in the presence of DNA damage. It induces apoptosis or cell cycle arrest which allows cells to repair themselves. Tuberin (TSC2), another tumour suppressor protein, regulates the G2/M transition in the cell cycle and negatively regulates protein synthesis and cell growth. Mutations in tuberin can lead to the multisystem autosomal dominant disease known as tuberous sclerosis (TSC). Previously, our lab has shown that Tuberin regulates mitotic onset through cellular localization of the G2/M Cyclin, Cyclin B1. My project focuses on the Tuberin/Cyclin B1 complex in relation to G2/M arrest and DNA damage repair. In this study, we will overexpress Tuberin-WT and Tuberin clinical mutants in NIH-3T3 (mouse) and U2OS (human) p53 wild type cells. Etoposide, a topoisomerase II drug, will be used to induce DNA damage. Cells will then be analyzed by flow cytometry, TUNEL assay, and western blot to assess their cell cycle profile, apoptotic levels, and protein expression. Using CRISPR-Cas9 technology, a NIH-3T3 null TSC2 cell line will be created to clarify the role of Tuberin during DNA repair. Preliminary results have determined that 4μM of etoposide treatment at 8 hours arrests 50% of NIH-3T3 cells at G2/M. This project will provide greater insight into DNA damage induced carcinogenesis, TSC, and other proliferative diseases.

“Joining the Porter lab in my first year has been one of the most rewarding experiences of my undergraduate career. Not only was I able to learn about advanced scientific techniques in class, but I was able to put them in action throughout my own research in lab. The problem-solving, critical thinking, and hands-on techniques I learned during my thesis are skills that I will carry forever. I was also lucky enough to make life-long friendships during my research journey. There were some challenging moments, but I could always rely on my lab team members and mentors to guide me. The last three years have been an amazing experience, and I wish the best for the next team of brilliant undergrads.”

The Essentiality of Spy1 in Cooperation with Hepatocellular Carcinoma Drivers to Promote Tumour Formation

Liver cancer is the fourth leading cause of cancer-related deaths worldwide, standing at an estimation of 800,000 deaths annually. Among the various subtypes, hepatocellular carcinoma (HCC) is the most common primary liver malignancy. HCC is known to develop through a series of genetic and epigenetic alterations of proto-oncogenes and tumour suppressor genes in the liver environment. These changes ultimately lead to the malignant transformation of hepatocytes, the primary cells of the liver. Various HCC drivers are known to cause disruption of cellular pathways and promote tumour formation. Importantly, several cell cycle mediators cause dysregulation, thereby stimulating tumour formation and progression. The cyclin-like protein Spy1, promotes cell cycle progression and overrides apoptosis. Recent reports have detected increased levels of Spy1 in human HCC, which directly correlates to severity of the disease and poor prognosis. We hypothesize that Spy1 plays a critical role along with hepatocellular carcinoma drivers to advance tumour development.  We will test the essentiality of Spy1 on HCC development by first investigating potential gRNAs to use for Spy1 knockout in vivo in the liver, for hydrodynamic tail vein injections in wildtype mice. Simultaneously, in vitro testing of HCC cells (HepG2) will study the importance of Spy1 in HCC cell characteristics in combination with HCC drivers such as c-Myc, p53, and 𝛽-catenin. This project will assist in understanding the essentiality of Spy1 in HCC, which may reveal insight into the molecular mechanism of the tumour suppressors and proto-oncogenes connected with this subset of liver cancer. 

“Applying to Porter lab during the start of my second year was genuinely a spontaneous decision but it turned out to the best decision I’ve made in my life. Before joining the lab, I had no idea what I wanted to do after graduating but after stepping foot into Porter Lab, I was able to unlock my passion for research. My time in the lab learning new skills, meeting peers from various walks of life and finally executing my undergraduate thesis made me realize the potential for myself to pursue a career in research. I have learned an incredible amount of information during the years and the passion to learn continues to grow. I learned to appreciate research as not just a career but as a lifelong passion which at times is underapprecaited. It may be time consuming, require numerous amounts of trials and errors and force you to step out of your comfort zone but the journey is worth it. I was privileged to work alongside such an amazing team of research assistants and colleagues that supported me at every point of my journey. Seeing how much investment is made into cancer research, and how much of an impact every single attribute plays into the final goal, makes me realize that I chose the correct path and I can’t wait to delve more into it. The Porter lab has wonderful incoming students that will continue to make the lab’s name shine, can’t wait to see what more they can accomplish. I will always cheer on for the lab and its members!!. “

2021 Undergraduate Theses – Kate, Kim, and Sami

fidalgo — Mon, 03 May 2021 16:40:38 +0000

Our 2021 undergraduate students have done wonderful work presenting their research results at the Ontario Biology Day, UWill Discover, and our Undergraduate Research Colloquium. Our lab has faced many challenges during this past year, the pandemic has tested our limits in many ways, but we are keeping up with our outstanding research projects. We had 5 undergrad students, some of them worked from home, while others were able to go to the lab, in one way or another we made sure they had the best research experience possible under these circumstances. As you can see below and here, they really enjoyed their time in our group.

Katie Zuccato

The Effects of Dexamethasone on Breast Cancer and Chemotherapeutic Treatment

Breast cancer is the second leading cause of cancer deaths in Canadian women. A particular aggressive subset of breast cancer, triple-negative breast cancer (TNBC), accounts for approximately 15% of all breast cancer diagnoses. Unlike other subtypes, it does not express well-defined molecular targets, such as hormone receptors, that allow for targeted treatment. TNBCs are therefore treated with cocktails of potent but general cytotoxic chemical therapies which have been known to cause harsh side effects such as hypersensitivity, nausea, and vomiting. These side effects are combatted by the addition of the synthetic glucocorticoid, Dexamethasone (Dex) to the treatment regime. It is of clinical significance to understand the impact of Dex on breast cancer behavior and how it influences chemotherapy treatment and patient response. Through the completion of a literature review, the role of Dex in promoting breast cancer progression through cell survival and metastasis was evaluated. Understanding the effects of glucocorticoids, such as Dex, on breast cancer cell biology and their interaction with chemotherapeutic agents can lead to alternative therapeutic strategies and improved patient outcomes.

“Joining the Porter Lab in my second year was a highlight of my university experience. Not only did I get to meet such talented and inspiring people, but I got to learn several skills that are applicable to many life situations. Even though my thesis project was unconventional due to the pandemic, I had such amazing mentors that ensured I learned as much as I would have if I had been able to physically be in the lab. I am grateful for the experience and the people that helped me succeed, and I am honored to have witnessed the many successes of my fellow lab members. I am looking forward to continuing to hear about the amazing work the Porter Lab Team is doing.”

Katie will be starting Optometry School at Waterloo University next fall.

Kim Nguyen

The Tumour Suppressor Tuberin: Coordinating DNA Damage and Mitotic Onset

The cell cycle is a series of events that involve cell growth and division. It is regulated by cyclins and CDKs, as well as checkpoints that control its progression. Tuberin (TSC2 gene) is a tumour suppressor protein that controls cell growth and proliferation. Tuberin mutations are implicated in several cancers and diseases such as tuberous sclerosis complex (TSC), a multisystem genetic disorder that is characterized by the growth of hamartomas. Previous data from our lab has demonstrated tuberin’s role in controlling mitotic onset by binding to the G2/M cyclin, Cyclin B1 according to nutrient availability. My project explores the role of the tuberin in the G2/M transition during DNA damage repair. DNA damage can result from events such as radiation, X-ray, and reactive oxygen species which activates the G2/M checkpoint to restrict mitotic onset and ensure sufficient time to repair damaged DNA. In our studies, NIH3T3 p53 positive cells were transfected with TSC2-WT or clinical TSC2 mutants that present low affinity for cyclin B1 (C696Y) or lack a GAP domain. The transfected cells were treated with etoposide, a topoisomerase II drug that induces double-stranded DNA breaks during the G2/M transition. The changes in cell cycle phases were analyzed using flow cytometry. Our preliminary results have determined that following treatment with 2µM of etoposide at 8 hours, there is a significant decrease in the % of cells at the G2/M transition in C696Y transfected cells vs. those overexpressing tuberin. This project will help expand the role of tuberin during the mitotic onset and clarify mechanisms of proliferative diseases such as TSC and cancers.

“My experience in the Porter Lab has been one that has been truly life-changing! By deciding to embark on this journey, I had the opportunity to really see science in action! Throughout our undergraduate career, we learn about these concepts and different experiments from listening to lectures and reading textbooks. Being able to go into the lab and perform my own experiments has shed light to truly how hard and rewarding science can be. The feeling of finally seeing the hard work pay off from repeating and troubleshooting an experiment countless times is one that is so fulfilling! While starting my 420 and performing my own research had its challenging moments, I was constantly supported and reassured by the rest of our lab every step of the way. My experience as a Porter Lab Rat has given me the opportunity to meet and work with so many amazing people. From Dr. Porter to the RAs, grad students, and other undergrads, everyone has been so passionate and dedicated in our pursuit of scientific advancement and it has been an honor being able to work with everyone. Joining the Porter Lab and doing a 420 has been such a gratifying learning experience for me and I highly encourage others to do the same!”

Kim is the recipient of the 1st place 10 Min Presentation for Cell and Genetics at the Ontario Biology Day. She will continue her research in our lab while coursing the 5th year undergrad studies at the University of Windsor.

Sami Alrashed

The impact of HA-labeled nanoparticles on CD44+ Tumour Initiating Cells in Glioblastoma

Glioblastoma (GBM) is the most aggressive brain tumor with a median survival of only 15 months. Despite decades of research, GBM continues to pose a great therapy challenge due to its extreme genetic and phenotypic heterogeneity. The pools of stem-like tumour initiating cells (TICs) maintain and recapitulate the heterogeneity of GBM; their ability to self-renew fuels resistance to treatment and tumour recurrence. Furthermore, successful treatment of GBM is hindered by the poor penetration of the available therapeutics through a tightly regulated blood-brain barrier (BBB). Conjugated polymer nanoparticles (CPNs) are a class of nanotechnology of potential novel application for GBM treatment. CPNs can penetrate the BBB and can also be encapsulated with drugs for cargo delivery, in addition to functionalizing their surface with ligands complementary to protein receptors expressed on the glioma cell surface. In collaboration with the Rondeau- Gagné group, my project focuses on a diketopyrrolopyrrole (DPP)-based CPNs labeled with a fluorescently tagged hyaluronic acid (HA). HA is the primary ligand of the CD44 receptor present on the surface of TICs. CD44 overexpression is implicated in GBM progression and correlates with poor patient survival. Using the human U-251 MG GBM cells and patient-derived primary lines, I will investigate the effects of CPNs on CD44 signaling and stem cell properties of TICs in vitro as well as in vivo, using a Zebrafish model. Collectively, these results will not only further validate the CPN system as a potential future anti-GBM therapy but also contribute to a better understanding of CD44 biology in GBM.

“When I joined the Porter Lab at the start of my second year, I had no idea that it would end up being both the highlight of my undergraduate journey and the most rewarding experience I’ve had to date. Before joining the lab, I wasn’t familiar with the research at all, but by the end of my fourth year, it’s safe to say that research has become a genuine, lifelong passion of mine. My time in the lab has made it clear that I want to pursue a career involving research in the future. It’s been an opportunity for me to both learn and develop many valuable skills and traits like working as a team, problem-solving, and patience, as well as responding to failure and keeping determination. I’ve learned an incredible amount of information during my time in the lab and the desire to learn only continues to grow. Research can be very time-consuming, and it does require a lot of dedication and effort, but I can confidently say that I’d repeat my experience in the Porter Lab over and over again with no complaints. The time I spent here has felt like my family away from home. A big part of my research experience revolved around building relationships with my mentors, graduate students, and fellow lab mates, and it has been a surreal experience. These are relationships that I’ll be beyond grateful for forever; I’ll always remember being a Porter Lab Rat. I’ve caught myself thinking about how amazing it is to be able to contribute to cancer research and work towards elevating the health of our community. Even if my actions seem minuscule, I recognize now that these little steps are all vital in understanding the bigger picture. The Porter Lab is in good hands – I know every individual member is going to make some very important contributions to the field of research, and I hope I can be there to celebrate these accomplishments with them all!”

Sami is the recipient of 1st place undergraduate speaker at UWill Discover conference, NSERC USRA 2020 summer, and 2021 summer. He will continue his research in our lab during the summer.

Happy Holidays 2020

fidalgo — Tue, 22 Dec 2020 21:16:51 +0000

Producer and Director – Our fabulous graduate student Isabelle Hinch.

Porter lab in quarantine – part 1

fidalgo — Fri, 17 Apr 2020 16:07:58 +0000

Part of the world has stopped because of the COVID-19 pandemic. Our lab is still pretty active during this time. We aren’t at the bench doing experiments, but we are at home working on papers, grants, catching up with our scientific reading and trying to release the stress of this difficult time by being creative with a few at-home projects.

One of these projects is making videos to share during our online meetings. It’s a way to cheer each other up and stay in touch!

Here are two videos from members of our lab. The star on the first one is our PI – Lisa and the second one features our Ph.D. student Adam. We hope you enjoy them and stay tuned for more videos.

Porter Lab at WCRG 2018

fidalgo — Sun, 18 Nov 2018 21:27:09 +0000

The Porter Lab was a success at the WCRG2018 this weekend. Our lab marked presence with one of nine Rapid Fire Session presentations and had a total of 10 posters presentations from a total of 58 conference posters. One of our students received a Student Research Excellence Award for his poster presentation and a Porter Lab alumni also received a Student Research Excellence Award for her poster presentation.

Dr. Lisa Porter

Dr. Bre-Anne Fifield presenting her research on liver cancer at the Rapid Fire Session

Adam Pillon – recipient of the Student Research Excellence Award presentation for his research on the Tuberous Sclerosis Complex

Alex Rodzinka

Dr. Bre-Anne Fifield

Carleigh Ross

Dr. Dorota Lubanska

Dr. Elizabeth Fidalgo

Fatima Nadeem and Isabelle Hinch

Frank Stringer, MD

Jackie Fong

Martin Bakht

Marisa Market – Porter Lab alumni, recipient of a Student Research Excellence Award for her research at the University of Ottawa where she is an MD-PhD student

Thanks for visiting and please leave comments below.

Introducing the Porter Lab Logo

fidalgo — Tue, 23 Oct 2018 19:27:47 +0000

The Porter Lab new logo was designed by our talented Ph.D. student Martin K. Bakht. The logo depicts the main research areas of our lab.

The P of Porter shows the following:

Asymmetric Cell Division

Speedy Cell cycle

The L of Lab shows the following:

DNA technology

Zebrafish used by our Lab as a xenograft model

The colours match the University of Windsor, Windsor Hospital and WCRG logos, connecting research and health care.

Hope you enjoy our new logo, please leave your comment below.

Elizabeth Fidalgo, Ph.D

Cancer Happens – TEDx Talks

fidalgo — Sun, 27 May 2018 17:01:22 +0000

Dr. Lisa Porter was invited to participate in TEDx Talks in Windsor (TEDx Windsor), an event to stimulate conversation and connections, helping communities and organizations.

One more time Dr. Porter made us proud!

Here is the video of her brilliant talk.

Please leave your comment below.

Elizabeth Fidalgo, Ph.D