Pretty much half of us is going to get cancer. This is part and parcel of our stressful lifestyle as well as aging. Some substances around us are very efficient in causing cancer. But why is that? Why some chemicals are able to cause cancer, which occurs when errors happen in our own cell division? Scientists from the Universities of Edinburgh and Cambridge decided to investigate this question.
Carcinogens – materials and particles that promote carcinogenesis – formation of cancer. Some carcinogenic substances find their way into our food, while others linger in our environment. Asbestos, for example, was used to make roofs and water pipes, but it is a strong carcinogen. And so are NOx emissions from diesel cars. And, of course, there are carcinogens in tobacco products, but everyone knows that.
Scientists observed the unique mutation patterns that occur when carcinogens cause carcinogenesis. They traced this mechanism back to the point where the tumour started developing. This allowed them to identify specific combinations of mutations that will create cancer cells.
In simple terms, carcinogens cause cell damage. If it lingers long enough, it is inherited when cell divides. Certain types of cell damage prevent cell’s replication machinery to read DNA sequences correctly, providing a chance for new mutations to appear. As more and more of these mutations happen, the chances of some of them being cancerous increase.
Burnt food, tobacco smoke, exhaust gasses, UV light and many other factors can contribute to the development of cancer. The problems occur when the damaged cells linger for too long, allowing for that damage to be inherited. As scientists now know, these carcinogens help damaged cells to dodge body’s natural immune system and eventually they become resistant to cancer drugs. Understanding the mechanism behind this process could lead to new treatment and prevention options.
Dr Duncan Odom, one of the authors of the paper, said: “The concept of lesion segregation helps us better understand how the surprising complexity of mutations in cancer cells can arise. It may help explain how cancer cells can react so flexibly and, in turn, shape cancer genome evolution”.
Scientists say that understanding of this mechanism could lead to new treatment options. Understanding the origin of the tumour could help selecting the most appropriate course of medication, dosage and other treatment properties. But it could also help avoiding carcinogens, because we will eventually know more about how they damage our cells.
Source: University of Edinburgh