The dramatic relationship between tobacco use and lung cancer it is more than clear. Just look at the number of measures that have been devised in recent decades to reduce both direct consumption and indirect smoking for sharing rooms with smokers. The problem is that there are other risk factors that cannot be controlled as easily as tobacco use. This is the case, for example, of the environmental pollution. It can also increase the chance of developing lung cancer, although the causes have not always been clear. Now, thanks to research presented this weekend in the Congress of the European Society for Medical Oncology (ESMO)we know better that relationship.
And it is that, according to its authors, from the Francis Crick Institute and University College Londonthe key is in a mutation that is active in the presence of polluting particles. Specifically, they are the smallest particles, known as PM2.5, which seem to have a greater influence. These come from the consumption of fossil fuels, the same ones that also enhance the greenhouse effect. But in this case it is a very different effect.
The study that demonstrates this also points to a inflammatory mediator substance as one of the main actors in this terrible effect. Therefore, not only the importance of reducing pollution levels is demonstrated. A target to which some specific treatments could be directed is also described.
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The authors of this study initially focused on a mutation in the EGFR geneknown to be present in about half of people with lung cancer who have never smoked.
Both this and other types of cancer have a high genetic componentbut also environmental. For this reason, on this occasion they reviewed the medical records of people residing in different points of UK, South Korea and Taiwan, in search of some environmental trigger that could increase the effects of this mutation. And they found it.
In fact, they found that the probability of developing cancer was quite low in those people who had the mutation and lived in places with little pollution. In contrast, those exposed to very high levels of PM 2.5 particles were much more likely to develop non-small cell lung cancer. In addition, this effect was detected in a second mutation, located in the gene KRAS.
This shows that, in this case, the environment, beyond tobacco, is paramount. It goes without saying that both mutations, which usually appear in lung cells as a result of aging, were not in themselves as dangerous as once thought.
A target to attack when there is pollution
Another fact that caught the attention of these scientists is that, in people with these mutations, pollution also triggers the influx to lung cells of macrophages. These are cells of the immune system, whose role is to go to damaged cells or foreign agents and ingest them to prevent them from causing damage to the body. said very roughlyThey eat the enemy. The problem is that they also release proinflammatory substances which can become quite harmful if they accumulate. It is the case of the interleukin-1βwhich in this case is doubly harmful, since it promotes the expansion of cells affected by the EGFR mutation exposed to contamination.
The good part is that if this substance is blocked, it could stop the progression of lung cancer. For this reason, these scientists are already working on the study of possible drugs directed at this target. In fact, their study is consistent with the results of previous research, in which an improvement in the prognosis of lung cancer patients treated with antiinterleukin-1β antibodiesdirected to take her off the stage.
Logically, the best thing would be to look for new ways to reduce the use of fossil fuels. Thus, the problem would be nipped in the bud. Meanwhile, it does not hurt to act against its consequences.