Samer is a biology student at the University of Windsor. With his 2014 – 2015 research studentship, he will work with he will be working with Dr. Lisa Porter at the Windsor Cancer Research Group on a project focused on brain cancer treatments.

Samer’s project has been generously funded by Diane Cameron and Nexen Energy, Calgary AB, in Memory of Edward Zdanowicz

About the Research

Project title: Role of Spy1 in Neurogenesis; Implications in the Development of High Grade Glioma

Project description

Brain and neural-derived cancers are the leading cause of cancer-related deaths from solid tumours in children and are among the most aggressive forms of cancer. Populations of cells resembling normal neural stem cells are capable of initiating neural tumour growth and promoting drug-resistant relapse in patients. The Porter lab has characterized a protein that is normally important in the division of neural stem cells. This protein is found at high levels in select human brain cancers and correlates with poor patient outcomes. The Porter lab has developed a mouse model to study the effects of high levels of this protein at select stages of brain development. This project will generate tools that aim to improve initial diagnosis and open up new avenues of therapy. Brain cancers result in approximately 36,000 years of life lost to Canadian citizens annually, finding new ways to effectively treat these patients is of high priority.

Over the course of two summers, Samer will learn mouse genetics which involves crossing different mouse lines, genotyping, and tagging and documenting all genetic information. He will aid in generating lines of mice where the Spy1 protein has been turned on at select stages of brain development. He will aid in collecting tissues for pathology and live cell samples for stem cell analysis. He will learn some classic techniques for studying the characteristics of neural stem cell populations.
Samer will also work with Drs. Lubanska and Stringer to determine whether timing of brain tumour initiation alters the populations and characteristics of neural stem cells driving tumours to grow. He will also determine whether stage of development alters the sensitivity of the mouse models to chemotherapy treatment.

About Samer, in his own words…

Being awarded a Brain Tumor Research Studentship means that not only will I be able to conduct research on brain tumors, but also make a difference in the world today.  I am thrilled and honored to be the recipient of a Brain Tumor Research Studentship and would like to express my sincere thanks to the donors for making this award possible. This award will greatly facilitate my ability to conduct research in the field of cancer biology and will allow me to focus on my career as well as intellectual development.

My interest in the field of cancer research is largely a result of my passion for education. Education has the power to make the world a better place. In order to be successful in the field of research, one must be a continual learner. The reason I enjoy research very much is because I love learning new things. By receiving this studentship award, I can assure you that not a single day will pass without learning something new which is why I will make the very best of this experience.

Overall, receiving this award has been a step forward for me in life and has given me an opportunity to explore my options in the field of cancer research while making a difference in the world today. I am extremely excited to get started on my project this summer and look forward to making a difference one day at a time.

Project Update

Thanks to your generosity and support, over the past summer we have begun utilizing our Zebrafish model to examine and analyze the effect of Spy1 on the metastasis of glioblastoma cancer cells. We have determined that the glioblastoma cell line is in fact invasive predominantly when Spy1 expression is up-regulated. Conversely, when Spy1 expression is knocked-down, we observe a drop in the invasiveness off the cancerous cells. Methods such as qRT-PCR were used to ensure that levels of Spy1 were up-regulated or knocked-down. Furthermore, this summer has allowed me to obtain valuable laboratory skills including: culturing cells, running gels, injecting Zebrafish, breeding Zebrafish, proper assembly of shrimp hatchery, imaging using a Leica microscope, and image analysis using a program called ImageJ.

Read more from Samer’s midpoint report…

About my experience

Overall, I am very honoured and fortunate to be given this opportunity. I am looking forward to working in the lab next summer and cannot wait to get started. I would like to thank the Brain Tumour Foundation of Canada for this monumental opportunity. Without your efforts and financial support this would not have been possible, and I am truly thankful.

Final Report:

As a result of your continued support and generosity, over the past summer we have continued to study the efficacy of targeting cell cycle regulators in the treatment of medulloblastoma (MB). The objectives of our study were two-fold: (1) we conducted studies to determine if the atypical cyclin-like cell cycle protein, Spy1, was present in the sonic hedgehog (SHH) subtype of MB, and (2) we studied the role of Spy1 on the effectiveness of specific cyclin-dependent-kinase inhibitors (cancer therapeutic agents).

We first analyzed protein expression in two SHH MB cell lines. Our results showed that Spy1 protein is expressed in SHH MB. Additionally, further data suggested that Spy1 levels are elevated in the tumour initiating cell population and that Spy1 may be required for their self-renewal. When MB cells with Spy1 protein knockdown were injected into the brain of a Zebrafish model organism, a decrease in the number of tumour cells was noted in comparison to cells that were injected without the knockdown. Lastly, when we treated the injected cells with a synthetic cyclin-dependent-kinase inhibitor, the cells with Spy1 knockdown exhibited greater sensitivity to the inhibitor as compared to the cells without Spy1 knockdown. Thus, these studies have provided evidence suggesting that Spy1 may potentially be playing a role in the tumourigenesis of MB.

Read more from Samer’s final report.

About my experience:

I have been very fortunate to conduct research for such an amazing Foundation. Throughout the years I have grown as a scientist both intellectually and physically in a positive and supportive environment. Additionally, I have come to appreciate the field of science and the hard work that goes into producing great results. My deepest gratitude goes to Brain Tumour Foundation of Canada and to all its donors. Without your support I would not be where I am today. Thank you very much for all of your kindness and assistance.