From Basic Biology to Cancer Research

Early in my scientific career, my attention was drawn to the basic mechanics of cell growth and division. I was fascinated by the precision required to maintain tissue health and function. As my work progressed, a clear connection emerged between these fundamental processes and the development of cancer.

The same systems that allow the body to repair itself can, conversely, drive disease when regulation breaks down. That understanding redirected my research toward focusing on where and how that balance is lost.

Helping build the WE-SPARK Health Institute has been one of the most meaningful parts of this mission. What began as a local effort has grown into a collaborative health research network connecting universities, hospitals, clinicians, and community partners across the Windsor-Essex region. Watching ideas move from discussion to discovery and then toward patient impact has reinforced the power of working together.

The Line Between Repair and Disease

One of the successes from my lab is understanding the roles of a protein called Spy1, which is elevated in several different aggressive cancers, including breast, liver, prostate, and brain cancers such as glioblastoma, and has the potential to be a novel target for more personalized, directed therapy.

As a recent example of this work, we wanted to understand the role of Spy1 in healthy brain tissue, long before a tumour forms. To do this, we focused on adult neural stem cells, which support learning, memory, and brain repair. We found that when Spy1 levels were increased in these cells, they persisted longer and divided more often. At first glance, that might sound beneficial. The results told a different story. The excess activity disrupted normal brain cell balance, interfered with learning, and created conditions that favoured abnormal growth.

These are the kinds of early changes that, over time, can increase vulnerability to cancer. This work revealed just how narrow the line can be between normal repair and disease. Even small shifts in cellular control can have lasting consequences, especially in tissues as complex as the brain.

The Importance of Working Together

Breakthrough research doesn’t happen alone. I have seen firsthand how progress depends on collaboration. My involvement with national funding agencies, such as the Canadian Institutes of Health Research, has given me a stronger appreciation of how national research priorities are set and how that support shapes what is possible in both the lab and the clinic. Serving on the board of Research Canada has also emphasized the importance of strong advocacy to sustain cancer and health research across the country. Working with charitable organizations and patient-working groups has reinforced that the most meaningful research is that which is shaped by the very people it aims to serve, ensuring our scientific efforts translate into better lives for patients and their families.

These experiences continue to shape how I think about progress. Real momentum occurs when scientists, clinicians, policymakers, patients, and communities come together, share ideas, and move forward with a common goal.

Shaping the Future of Cancer Care

Progress toward better cancer treatments is driven by patience, persistence, and a willingness to learn from unexpected results. Some discoveries answer long-standing questions, while others open new ones. Both move the field forward.

Research lays the foundation, collaboration gives it strength, and together they shape the path toward better cancer care. When discovery, clinical insight, and shared objectives come together, they create an environment where ideas move more freely, questions deepen, and understanding continues to evolve.

In my lab at the University of Windsor, my team has been investigating the role of the Spy1 (Speedy) protein, a cell-cycle regulator, in aggressive brain cancers like glioblastoma, one of the most aggressive and difficult-to-treat brain cancers. Our recent work has provided new insights into how Spy1 affects neural stem cells, which are critical for brain repair and regeneration, and how this relates to cancer progression.

Spy1’s Impact on Neural Stem Cells

Neural stem cells are essential for memory, learning, and the brain’s ability to heal itself. As we age, the number of active stem cells in the brain naturally decreases, which impairs its regenerative capabilities. Spy1 has been shown to play a key role in neurogenesis by activating these stem cells, potentially aiding in brain repair.

However, we discovered that too much Spy1 causes problems. In our studies, we genetically engineered mice to overexpress Spy1 specifically in their neural stem cells. While this activation increased the number of stem cells, it also caused them to divide uncontrollably, which made them more susceptible to becoming cancerous. This was a critical finding, as it sheds light on how glioblastoma cells might develop from stem cells that have gone awry due to Spy1 overexpression.

Learning Deficits and Aging

Our research also revealed some unexpected consequences. Initially, we thought increasing neural stem cell populations might improve learning and memory. Despite the increased number of stem cells, the mice showed learning deficits. This shows that simply increasing stem cells doesn’t always improve brain function. In fact, it may even disrupt other important brain cells, leading to cognitive issues.

In addition to its role in cancer, Spy1 also appears to influence brain aging. We found that increasing Spy1 levels in mice helped maintain neural stem cell populations longer than in normal aging, which could have implications for treating neurodegenerative diseases like Alzheimer’s. However, this too must be carefully controlled, as promoting stem cell expansion without understanding the full implications can have unintended side effects.

A Path to Better Treatments

Our findings suggest that targeting Spy1 could offer a new approach to treating brain cancers such as glioblastoma. By carefully controlling Spy1 levels, we might be able to enhance brain repair without triggering excessive cell division that can lead to cancer. The challenge now is to figure out how to selectively target Spy1’s activity in a way that benefits brain health without promoting tumour growth.

A Collaborative Effort

This research has been a collective effort, and I’m grateful for the talented team that continues to work alongside me. In addition to my work at the University of Windsor, I’ve had the privilege of contributing to cancer and health research in different roles throughout my career, including formerly serving as the founding Executive Director of WE-SPARK Health Institute, a collaborative network of researchers, clinicians, and community partners across the Windsor-Essex region.

My work has also been supported by national research organizations, including the Canadian Institutes of Health Research (CIHR), and I serve on the board of Research Canada, where I advocate for advancing cancer and health research across the country.

Looking Ahead

The findings from our research are just the beginning. By continuing to study the balance between Spy1, neural stem cells, and cancer progression, we hope to develop targeted treatments for glioblastoma and find ways to improve brain health as we age. These efforts represent an exciting step toward a better understanding of cancer and more effective treatments for complex brain diseases.