- The researchers screened lung cells from smokers and non-smokers for the mutations.
- They found that smokers tend to have more mutations in their cells than non-smokers.
- They also found that the frequency of mutations did not differ significantly between heavy smokers and less heavy smokers.
- They suspect DNA repair mechanisms may underlie this, but say more research is needed.
Lung cancer is
For decades, researchers have suspected that carcinogenic chemicals in cigarette smoke damage DNA and lead to
However, limitations in the study and design methods mean that to date, this theory cannot be definitively proven because there is no way to accurately measure mutations in normal cells.
Recently, researchers from Albert Einstein College of Medicine, Bronx, New York, used new methods to assess genetic mutations between lung cells in heavy smokers and people who do not smoke.
They found that smokers had significantly more lung cell mutations than non-smokers. However, heavy smokers had no more spikes than heavy smokers.
The study was published in
For the study, the researchers took lung and airway cell samples from 33 individuals, including:
- 12 adults with no smoking history between the ages of 18 and 86
- 2 teenagers with no smoking history
- 19 smokers, including 7 former smokers and 12 current smokers, aged 44-81 years
Smokers reported smoking cigarettes between 5.6 and 116 pack years. One year is equivalent to 20 cigarettes per day for one year.
The researchers noted that 14 out of 19 smokers were diagnosed with lung cancer along with a non-smoker.
To analyze the cells, the researchers used single-cell multiple displacement amplification (SCMDA). They developed SCMDA in
Ultimately, the researchers found that human lung cell mutations accumulate with age and that smokers have more mutations than non-smokers.
However, they noted that they did not observe statistically significant numbers of mutations in cancer-causing genes such as Notch1 as a
They say this was not an unexpected result because the mutations occur randomly, and because only three to eight cores were analyzed for each individual. They say that more in-depth analysis could lead to different results.
Their most interesting finding, they report, is that levels of mutation frequency stop after 23 years of cigarettes. This means that heavy smokers did not necessarily have more spikes than lighter smokers.
They further said that this phenomenon is not related to the occurrence of cancer, as the frequency of mutations in cancer patients is not significantly different from those who did not have cancer.
To explain why the frequency of mutations has stabilized after 23 bundle years, study co-author Dr. Jan Vig, professor and chair of the Department of Genetics at Albert Einstein College of Medicine, said, Today’s medical news:
“Firstly, [some smokers] They could have better detoxification systems to take care of the mutagenic compounds in tobacco smoke before they can damage the DNA of the cell genome.”
Second, they could have super-DNA repair systems that take care of DNA damage and repair it quickly with only a few errors that usually cause mutations. We are particularly interested in this last possibility because we can test this using our methodology,” he explained.
The researchers say in the paper, however, that there is no available evidence of an ability to repair damage with minimal mutation burden.
However, to summarize their work, the researchers say their study shows that smoking increases the risk of lung cancer by increasing the frequency of genetic mutations.
They added that their findings may also explain why only 10-20% of smokers develop lung cancer and that this may be due to DNA repair or improved detoxification from tobacco smoke.
Ultimately, they say their study provides a rationale for further evaluation of lung cancer risk factors that modulate susceptibility to mutations in normal airway cells.
When asked about the limitations of their findings, Dr. Feig explained: “The most serious limitation is that we cannot detect all types of mutations. For example, large structural mutations that eliminate more than one or a few base pairs cannot be detected in single cells. using our method.
Perhaps there are not many such mutations, but they have a much more serious effect on the health of the cell. “We are working on such methods at the moment,” he added.
“[The researchers found] Mutations occur with age in [smokers and] Osita Onuga, a thoracic surgeon and associate professor of thoracic surgery at the Saint John Cancer Institute at Providence Saint John’s Health Center in Santa Monica, Calif., who was not involved in the study, said, MNT.
So, if you smoke, you should stop smoking to reduce your risk. But for non-smokers, other than trying to live a healthy life, it is unfortunately part of aging. He explained that the study did not address this topic.
When asked about the limitations, Dr. Onuga said: “The most glaring limitations are the sample size and the lack of age-matched cohorts.”