Illustration of chromosomes from a cancer cell showing large-scale alterations.

Charles Swanton : Cancer Evolution and Genome Instability Laboratory

We are studying how cancers evolve in the body to spread and become resistant to therapy and finding new ways to treat them more effectively.

In recent years it has become clear that every tumour is made up of many different groups of cancer cells, each with their own unique genetic makeup but all related to each other. Some groups of tumour cells develop resistance to treatments such as chemotherapy, immunotherapy, radiotherapy and targeted therapy, meaning that when the cancer comes back it is harder to treat.

This diversity, known as heterogeneity, occurs through evolutionary processes at work inside the tumour as the cells pick up DNA changes (mutations or chromosomal rearrangements) that allow them to respond and adapt to changes in the environment around them.

We are using the latest DNA sequencing technology to read the genetic makeup of cancer cells within tumours in ever greater detail, teasing out patterns of evolution (evolutionary rule books), cancer heterogeneity and working out what changes have happened as a tumour evolves. We’re also investigating the processes that cause mutations and accelerate tumour evolution and working out how they might be stopped. And we are running evolutionary clinical trials with immune and targeted therapies to bring the benefits of our work to patients as quickly as possible.

Understanding what drives tumour heterogeneity and mapping the evolutionary pathways at work as cancers evolve and change is essential if we are to treat cancer more effectively in the future.