While ovarian tumours often respond to initial treatments, many recur and become resistant to therapy. Historically, this has been viewed as a process of selecting for rare cells that have acquired mutations that provide protection against the treatment. However, increasing evidence suggests that this may not be the dominant mechanism of resistance.

Cancer cells are not static. Their traits are malleable and influenced by their local environment. As such, throughout the landscape of the tumour, diverse malignant cells populations exist—a phenomenon described as “intratumoural heterogeneity”. The properties of these cells affect their sensitivity to all forms of treatment, including chemotherapy, targeted therapies, and immunotherapies. Furthermore, this malleability allows cells to adapt to changes in their environment. We are particularly interested in understanding how cancer cells evolve following their exposure to treatment.

Is therapy resistance a property that only emerges after treatment onset? Can we predict resistance from the properties of cells prior to treatment? Importantly, can we develop approaches to restrict the malleability of these cells?

To study this, we use model systems derived from patient tumours and simulate treatment regimens in the lab. We’ve developed techniques to make millions of measurements to profile the diversity of cancer cells and track how they change throughout the course of treatment.

More info soon!