As part of the current standard treatment, most breast cancer patients receive a combination of chemotherapy and radiotherapy. Despite its success, still many patients gain little or no benefit from this treatment, as evidenced from the elevated rates of locoregional recurrence, distant metastatic spread, and breast cancer deaths. Unfortunately, those patients will nevertheless suffer the short and long-term side effects of the inefficient therapy. My ultimate aim is to develop patient-specific strategies that maximize the damage in tumor cells while minimizing the damage to normal cells.
After the chemo- or radiotherapy a fraction of tumor cells will die, some cells will remain quiescent, while other cells will survive and continue dividing. This is a characteristic response to cancer therapy known as fractional response, where a subpopulation of cells survives the treatment. My research focuses on studying the cellular events and signaling dynamics that control the heterogeneous cell fate response of individual cells in time. Specifically, how internal cycling factors, such as the circadian clock, the cell cycle, and the p53 protein dynamics interact with the DNA damage response pathway to determine the response to radiotherapy and chemotherapy in cancer cells.
I develop methods that combine long-term live single-cell microscopy with time series analysis and mathematical modeling to track the evolving internal cellular state and the outcome cell fate. Gaining understanding on the internal state and dynamics of cell fate decision of individual tumor cells will help us to identify sensitive cellular states and to design optimal schedules for future cancer treatments.