For our Director of Discovery Marion Cubitt it’s mutational burden – in other words, the genetic diversity of cancer cells: 

“When I started working in oncology it took a while to appreciate the magnitude of the task. I distinctly remember watching a conference talk on mutational burden and thinking – wow – I hadn’t appreciated that each cancer really is a parasite, a living thing that’s constantly changing.  

Coming from a microbiology background originally, there’s an obvious parallel between bacteria developing antibiotic resistance, for example, and a cancer trying to outrun its host’s immune system.”  

When we treat an infection with antibiotics, bacteria can develop resistance due to genetic mutations that alter their susceptibility to certain drugs. Similarly, in tumours with a high mutational burden, treatments targeting specific genetic mutations exert a selection pressure, leading to the emergence of subclones resistant to that treatment.  

In order to address this issue, we need to find a way to maximise the effectiveness of initial treatments. One way to do that is through early diagnosis – if the tumour cell population has less time to evolve, treatments are more likely to be successful. 

But if those cancer treatments do fail, every relapse can result in a more complex and diverse population of tumour cells. 

So, how do we tackle this challenge?  

We’ll be speaking with our expert team to delve deeper into the complexities of treating cancer, but we’d love to hear your thoughts on this topic as well. Make sure to follow us on LinkedIn so you don’t miss what our experts have to say!