For years, British physician and researcher Charles Swanton was asked the same question by patients in his office: “How can I get lung cancer if I don’t smoke?” A study was published Wednesday in the journal Science Nature Trying to better answer this question, which created a certain “puzzle” for scientists for a long time.
Air pollution by Fine particles – Contains exhaust fumes and gases from cars Fossil fuels – can trigger the amplification of pre-existing mutations in lung cells, leading to increased tumor growth, suggests a paper co-authored by Charles Swanton. Thus, non-smokers living in areas with high air pollution are more likely to develop lung cancer than those living in areas with low air pollution.
“The finding that lung cancer is associated with air pollution is not new. What is new here is the mechanism [biológico] An underlying cause that proves a causal relationship [entre as duas coisas]”, said Charles Swanton during a virtual press conference. The oncologist leads a research team at the Francis Crick Institute in London and is the medical director of Cancer Research UK in the United Kingdom.
Doctor/European Society for Clinical Oncology
A study of Nature Part of the atmospheric pollution – more precisely, fine particles with a size equal to or less than 2.5 micrometers (PM2.5) – interacts with lung cells, causing biological changes that lead to malignant tumors. The researchers focused on mutations in the EGFR or KRAS genes, which are more common in lung adenocarcinomas.
A team of scientists studied the association between PM2.5 exposure and the frequency of lung cancer in nearly 33,000 patients with EGFR mutant lung cancer from four countries (Canada, South Korea, the UK and Taiwan). Exposure to high levels of BM2.5 was associated with an estimated increased incidence of EGFR gene-mutated lung cancer, the study reported. However, it should be noted that the risk of lung cancer associated with air pollution is much lower than the risk associated with smoking.
Unique molecular signatures
“To determine how air pollution causes cancer, authors [Charles Swanton e colegas] “Analyzing the DNA sequences of tumors from non-smokers from polluted areas, the samples show certain genetic changes called point mutations, which are capable of activating genes that drive the growth of cancers,” says scientist Alan Balmain, a pioneer in this area of tumor biology, in a commentary published in the same journal. Nature.
The mutations found in the analyzed tumor tissue appear to be the result of natural processes (ie, genetic “mistakes” that occur during cell division) – unlike those found in the DNA of smokers’ tumors, where genetic changes are induced by tobacco. Smoke components. In other words, the mutations identified in samples from non-smokers have a molecular “signature” different from that of smokers.
Gabriela Gomez
Mutations in the EGFR and KRAS genes are often present in healthy lung tissue. They often result from natural aging processes in which cell division can create “failures” when replicating DNA. These genetic changes are “dormant” and only become a health problem when they are “awakened” by exposure to an environment with high levels of air pollution.
“Cells with multiple mutations appear to lie dormant in healthy tissues without causing any problems until they are ‘awakened’ by a process that transforms these cells into tumors early in development,” Alan Balmain writes in the article. .
The results were already announced at the most recent conference of the European Society of Medical Oncology (ESMO) in Paris in September 2022. Now, the authors publish the complete results of “adding new data” in an article published in the prestigious scientific journal. Nature.
Arousal of dormant mutations
The authors report that increasing levels of PM2.5 are associated with an estimated increased incidence of EGFR-mutated lung cancer. This association was verified, in the same article, by data from more than 407,000 individuals who are part of the British Biobank, a repository of human tissue samples, and by observations of a cohort of 228 individuals with lung cancer in Canada. . The team used animal models (mice) to investigate the cellular processes behind the development of lung cancer through exposure to PM2.5.
The authors incorporate these results into the study Nature To defend the idea that PM2.5 can act as a tumor promoter, an agent capable of “awakening” pre-existing cancer mutations. The team hopes that this new understanding of tumor biology will pave the way not only for preventive treatment approaches, but also for public policies that improve air quality.
“We are a laboratory dedicated to genetics, we grew up measuring mutations in DNA, and we have always assumed that genetic mutations are at the origin and progression of cancers. What these results show us is that there is a very important component connected to the inflammatory process that we have neglected. I assumed that these mutations [naturais] Not enough to trigger cancer”, explained Charles Swanton, responding to PÚBLICO in a virtual press conference.
When we think of cancers, it’s common to think of carcinogens—such as tobacco smoke—that cause tumors through direct DNA damage. In this particular case of lung adenocarcinoma, air pollution acts as a cancer promoter, “waking up” the already existing change. This new perspective, according to the British oncologist, really surprised the team during the investigation.
“Alan Balmain and other authors have already pointed out this inconvenient fact”, says Charles Swanton. “Our model is not correct for some types of cancer that develop in a complex way, and at the same time, mutations and a promoting agent must evolve,” concludes the British oncologist.
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