Grant: Travel Awards - Institute Community Support

Cancer arises when cells evade normal control mechanisms that limit their growth. One such mechanism is cellular senescence, a natural process in which damaged or stressed cells permanently stop dividing. Senescence acts as a powerful defense against cancer but the persistent accumulation of senescent cells with age can disrupt tissue homeostasis and promote chronic inflammation, thereby contributing to age-related diseases such as cancer. Understanding how this process works at the molecular level could lead to strategies that either activate or eliminate senescent cells, depending on the clinical context. My research focuses on two proteins, RUNX1 and ETV4, recently identified in our lab as key regulators of the senescence program. These proteins help "open" the DNA structure (chromatin) and activate genes that stop cell division. Interestingly, their expression is lost in pancreatic cancer cells, suggesting that shutting down this protective mechanism may help cancer progress. By studying how RUNX1 and ETV4 remodel chromatin to trigger senescence, we aim to uncover new drug targets capable of reactivating this fail-safe program in cancer cells. We are using cutting-edge biochemical, molecular, and genomics tools, including gene expression analysis, chromatin profiling, and pancreatic cancer models in the lab and in mice. Our ultimate goal is to develop new epigenetic therapies that restore chromatin openness, reengage the senescence program, and block cancer cell growth. This research will improve our understanding of how healthy cells prevent cancer and support the development of innovative therapies for pancreatic cancer, one of the deadliest forms of the disease. It also contributes to Canada's health research priorities by advancing novel anticancer epigenetic strategies and training the next generation of researchers.