Grant: Travel Awards - Institute Community Support

Lung cancer is the deadliest cancer in Canada and nearly all patients are treated with chemotherapy drugs that kill cancer cells. While these drugs work well initially, over time tumors adapt to escape their toxic effects, becoming resistant to chemotherapy. This state, known as chemoresistance, is a major barrier to improving lung cancer survival rates. My project aims to better understand the biology of chemoresistance to learn how to make chemotherapy treatment work better. One of the ways chemotherapies work is by triggering an antiviral response in cancer cells. Antiviral signaling is used by cells to defend against viral attack. The antiviral response produces signaling proteins called interferons that are toxic to cancer cells and help the immune system recognize and kill tumors. Interestingly, two proteins called YAP and TAZ can promote chemoresistance and block antiviral signaling, suggesting these two processes might be connected. However, it is not known whether YAP/TAZ promote chemoresistance by regulating antiviral responses. I hypothesize that blocking the function of YAP/TAZ will boost antiviral signaling in tumors and make chemotherapy more effective at killing them. To test this hypothesis, I will disrupt YAP/TAZ function and determine how this affects antiviral signaling triggered by chemotherapy treatment. I will also measure how this affects lung cancer sensitivity to chemotherapy treatment. The findings from my project could inform new strategies to overcome chemoresistance and increase the effectiveness of chemotherapy in lung cancer patients. Combining YAP/TAZ inhibitors with chemotherapy could enable lower doses of chemotherapy to be used in patients, which would reduce its toxic side effects and improve patient quality of life.