Smoking increases the risk of cancer. We have known for a long time. Now a new study has linked, for the first time, a wide variety of tumors to genetic damage to the organs and tissues of people who smoke. The research, led by scientists from the Los Alamos National Laboratory (USA) and the Wellcome Trust Sanger Institute (UK), has been published in the journal Science.
People who smoke are at risk for at least 17 types of cancer. However, despite this data, the mechanisms by which the genome is damaged by tobacco and ends up causing mutations that trigger cancer are unknown. New research has shown that tobacco increases the risk of cancer by causing mutations in tissues directly and indirectly exposed to smoke.
The researchers analyzed the genome of more than 5,000 human tumors of smokers and non-smokers, measuring the genetic damage caused in different organs of the body and describing the mechanisms that originate the DNA mutations. The findings revealed that smokers accumulated an average of 150 additional mutations in each lung cell – 97 in the larynx, 39 in the pharynx, 23 in the mouth, 18 in the bladder, and 6 in the liver cells. every year smoking a pack of cigarettes a day.
“Mutations associated with tobacco smoke are more complex than previously thought. Tobacco damages DNA in organs directly exposed to smoke and speeds up a mutational cellular clock in organs that are directly and indirectly exposed ”, explains Ludmil B. Alexandrov, co-author of the work.
In total, they found more than 20 traces of genetic mutations in the 17 types of cancer associated with smoking. However, of all of them, only five of these marks were really significant in cancers suffered by smokers.
“Organs that are not in contact with inhaled smoke do not have the same direct mutational signature that is seen in the lungs. However, there is another in all cancer cells that accelerates the rate of mutation in smoking cells. The more mutations a cell has, the more likely it is that one of them is in a cancer-causing gene and causes it, ”explains Alexandrov.
