Funding outcome

Cervical cancer is one of the most common cancers affecting women in Canada, and its rates are increasing despite vaccination and screening programs. The cancer cells often survive the standard chemotherapy and radiation treatments, leading to the recurrence and spread of the cancer cells to other body parts. As a result, newer and more effective treatments are required to improve cervical cancer outcomes. Two proteins called Wee1 and Myt1 help regulate cell division. They act as safeguards, allowing cells to repair DNA damage before dividing. Dr. Chan's lab has previously shown that blocking these proteins can be an effective cancer treatment, forcing tumor cells into mitotic catastrophe. They also found that increasing Myt1 helps cancer cells become resistant to Wee1 inhibitors, but we still do not know how cancer cells resist treatments that target Myt1 itself. We hypothesize that cervical cancer cells use internal survival signals to resist Myt1-targeted treatment, allowing them to stay alive even when treatment causes severe problems during cell division. To better understand the Myt1 resistance, we will change these survival signals in cervical cancer cells to see how they affect response to Myt1 treatment. We will also use drugs that block these signals to test whether resistant cancer cells become sensitive again. Finally, we will compare gene expression and protein activity between the resistant and non-resistant parent line. Understanding the Myt1 resistance mechanism in cancer cells can help us identify markers that predict which patients will respond to this therapy. This knowledge will help in developing more effective combined treatments that prevent resistance from occurring, ultimately improving the success rate of treatment of cervical cancer in women.