Pseudo-coloured scanning electron micrograph of an oral squamous cancer cell (white) being attacked by two cytotoxic T cells (red), as part of a natural immune response. Image credit: Rita Elena Serda, Duncan Comprehensive Cancer Center at Baylor College of Medicine, National Cancer Institute, National Institutes of Health (CC BY-NC 2.0)
The human body is made up of around 36 trillion cells and 200 different types of cells, each with a specialised role. For example, immune cells are crucial for fighting infections. They also act as the body’s first line of defence against internal threats, such as cancer.
Cells have intricate systems to control how often and how much they divide, ensuring a fresh supply of cells. When some of these signals are faulty or missing, cells can start to grow and multiply uncontrollably. This unchecked growth can form tumours.
Some immune cells can recognise cancer cells by certain proteins on their surface and mark them for destruction. This process is thought to eliminate many potential tumours before they become dangerous. This way, early cancer can be held in check for years.
However, cancer cells can evolve genetic changes that help them evade the immune system. In response, immune cells adapt to find new ways to identify these mutations. This creates an evolutionary arms race, with each side developing new strategies to outsmart the other. Eventually, cancer cells may acquire enough changes to grow unchecked, outpacing the immune system.
So far, it has been unclear whether the interactions between cancer and immune cells leave detectable genetic traces in the DNA of cells. By analysing the DNA of advanced cancers, researchers may be able to reconstruct how tumours interacted with the immune system in the past. These insights could reveal patterns that help predict a tumour’s future behaviour and highlight new treatment opportunities.
Wang, Morison and Huang built a computer model to study how cancer and the immune system influence each other over time. By examining mutation patterns in tumours, they were able to trace how strongly the immune system shaped cancer growth.
The results showed that when cancer cells develop certain mutations that make them more visible to the immune system, the immune system launches strong bursts of activity to eliminate them. In this way, the immune system can shape which mutations persist in a tumour. For example, cancer cells with many mutations are more likely to be detected and destroyed. Over time, these strongly targeted cancer cells – and the immune cells that attack them – tend to disappear from the population. However, in some cancers, this effect is much weaker, and the immune system has less influence over the tumour’s genetic changes.
A key challenge is understanding how cancer mutations arise in the first place. To make progress, researchers will need to combine large-scale population data with detailed single-cell data. This knowledge will be especially important for advancing immunotherapies and other precision cancer treatments.
