THE HOSPITAL FOR SICK CHILDREN (SICKKIDS)

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As a Coop Research Technician for the Taylor Lab at the Hospital for Sick Children (SickKids), I have  been exposed to the research and lab workplace where I do animal-based work, genotyping, image collection and processing using Transmission Electron Microscopes (TEM) and ImageJ respectively for my project. Since the first month of this work term, I have had the opportunity to extend and apply my knowledge of oncology (cancer) research as I presented at the 20th New England Science Symposium hosted by Harvard Medical School's Office for Diversity Inclusion and Community Partnership and the Biomedical Science Careers Program (BSCP)!

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Medulloblastoma (MB) is a malignant WHO Grade IV brain tumor; the most common of its kind in children. While extensive efforts have been made to treat the primary tumor, less research has focused on treating its metastases, which cause both morbidity and mortality in patients. In addition, 60-70% of patients are expected to survive after 5 years, survivors do suffer grave cardiovascular, hormonal, neurological and oncological effects to their bodies, thus pushing the need for more effective treatments for survivors beyond the triad current standard of care (surgical tumor resection, craniospinal irradiation and chemotherapy). Notably, MB metastases specifically grow in the leptomeninges, thus examination of the molecular and mechanistic dynamics behind dissemination will be essential to creating rational targets for metastatic MB. I thus aimed to explore "What molecular drivers and mechanisms support the metastatic dissemination of medulloblastoma into leptomeningeal space?" Through a literature review on MB leptomeningeal dissemination, I was able to create a comprehensive diagram highlighting the different cellular and molecular events involved during the progression of this cancer at the clinical level (ie. during metastasis). Specifically, Research has depicted two key routes of medulloblastoma metastasis – a hematogenous and cerebrospinal fluid (CSF) dissemination. Both ways appear to share steps in a common metastatic pattern: the invasion-metastasis cascade. Mechanistically, primary tumor cells dissociate from the cerebellum and intravasate the blood or enter the CSF. Tumor cells thereafter travel through the blood or CSF and extravasate or implant onto the leptomeninges respectively. For successful dissemination in a disparate microenvironment, tumor cells enhance CCL2 and/or C3 expressions to enhance inflammation and growth of metastases respectively, promoting leptomeningeal metastasis. Overall, this investigation encapsulated a mechanistic approach of medulloblastoma to metastasize into leptomeningeal space. As MB is a heterogenous disease (meaning made of multiple subgroups that are molecularly and clinically distinct from each other), my examination into the functional roles of pro-metastatic genes could allow targeted approaches towards treating MB metastases in the clinical setting, and thereby may provide greater opportunity to reach effective interventional and preventative treatments for metastatic MB upon diagnosis through personalized medicine.

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I presented my research to 5 students and 2 judges, allowing me to enhance both written and oral communication skills to a diverse science audience. This skill is so instrumental because it not only can be extend to the every day actions when I am in the workplace and need to discuss tasks with my Supervisors, but also enhances my ability to communicate effectively and thus connect with a new audience for future conferences, lab meetings and even during my Final Work Term Report!

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To summarize, this research not only gave me the opportunity to further explore the MB field, but further gain a lifetime experience for written and oral communication through knowledge translation of my work (attached below). I am excited and I look forward to more opportunities to connect with the scientific community!

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