Why is cancer so difficult to beat, you might be wondering. The main problem with cancer is that it arises from our own cells. We are all unique and special, but so are our tumors, which makes it difficult to deal with them at a population level. Unfortunately, the same drug might not have the same effect on two different people, even though they might have the same kind of cancer. As we wait for personalised medicine to develop in the future, scientists are currently trying to enhance our natural and already personalised defence mechanisms: our immune system.
In general, people associate the immune system with the body’s mechanism of defense against viral, fungal, and bacterial infections. But this is not all it does – it also fights back against cancer. There is plenty of evidence showing how important a role the immune system plays in keeping cancer at bay. People with immunodeficiencies, for example, are known to be more prone to develop tumors.
So, why does cancer emerge in a person with a healthy immune system? Cancer is the result of the uncontrolled growth of as little as one of our own cells. Since these cells replicate quite fast, they often acquire mutations that can make them resistant to current medication or even the detection of the immune system itself. More strikingly, some cancers have been shown to create a microenvironment in which they use some of the cells of the immune system to their advantage, providing them with more glucose (food) and oxygen to facilitate their growth. Apart from this comfort, cancer cells become invisible and thus protected from the rest of the immune system, which would otherwise eliminate them. More specifically, there are two families of cells belonging to the immune system that generally become cancer friendly: cancer associated-macrophages and regulatory T cells.
“Strikingly, some cancers have been shown to create a micro-environment, using the immune system to their advantage”
Cancer cells can therefore become reliant on these particular cell families for their survival. And so, researchers are currently working on ways to exploit this weakness. Individual disruption of the cancer-associated macrophages or the regulatory T cells has so far failed to provide any satisfactory results, the reason being that upon dysfunction in one of these cell families there is a tendency for the other to increase in terms of number and functionality. There seems, in other words, to be a compensatory effect.
With this in mind, researchers at the Babraham Institute employed a dual strategy in which they managed to disrupt both cell families simultaneously. In their recent publication, they show that in a colon cancer model in mice this treatment promotes the immune system rejection of the cancer. By the end of the study half of the mice were completely tumor free. Although much more research needs to be done, the inhibitor of the T regulatory cells they used is already approved as a treatment for some cancers, so this new strategy could potentially be easily translated into the clinic.
Considering how complex cancer is as a disease, boosting our own immune system to battle it is a strategy that might serve to overcome current limitations when the medications we do have stop working.