A few years ago, scientists demonstrated that our immune system could detect and eliminate tumour cells. Unfortunately, some tumours cells develop mechanisms that make them invisible to the immune system, and when this happens, the tumour grows and we talk about cancer. Scientists developed drugs which can block the mechanisms that allow the tumours cells to escape the immune system. When these drugs are given to patients with cancers, their immune system can detect the tumour again and eliminate it. The two scientists who developed the first drug that was capable of this are James Allison and Tasuku Honjo, and they received the Nobel Prize of Medicine in 2018 for this. This drug worked exceptionally well on some patients who were refractory to conventional therapies. Sadly though, for many patients, it did not work at all. Now many other similar drugs have been developed with the hope to cure all patients. They all block slightly different mechanisms which can be established by the tumour to escape the immune system.
To understand how these drugs work and which ones will be the best to use for which patients, we have to use pre-clinical models. Because these drugs are working by changing the effect of the immune system on the tumour, we have to work with a whole animal where these systems are present. Unfortunately, the models which we have been using in the lab for years are not useful for studying this kind of therapy. Lung cancer in human has many mutations, and this is these mutations that the immune system can detect to recognise the tumour and to eliminate it. The mouse models of lung cancer we have been using so far have no mutations and therefore, could not be seen by the immune system making them useless to study immunotherapy. This project aimed to induce mutations in mouse lung tumours to make them more similar to their human counterpart and to make the immune system of these mice able to see the tumours.
