From the Journals

Stopping smoking allows healthy lung cells to proliferate



New research results reinforce the benefits of quitting smoking.

Not only does it stop further damage to the lungs, it appears that it also allows new, healthy cells to actively replenish the lining of the airways. This shift in the proportion of healthy cells to damaged cells could reduce the risk for lung cancer, say researchers.

The findings were published online in Nature (2020 Jan 29. doi: 10.1038/s41586-020-1961-1).

The team performed whole-genome sequencing on healthy airway cells collected (during a bronchoscopy for clinical indications) from current smokers and ex-smokers, as well as from adult never-smokers and children.

The investigators found, as expected, that the cells from current and ex-smokers had a far higher mutational burden than those of never-smokers and children, including an increased number of “driver” mutations, which increase the potential of cells to become cancerous.

However, they also found that in ex-smokers – but not in current smokers – up to 40% of the cells were near normal, with far less genetic damage and a low risk of developing cancer.

“People who have smoked heavily for 30, 40 or more years often say to me that it’s too late to stop smoking – the damage is already done,” commented senior author Peter J. Campbell, PhD, Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton, England.

“What is so exciting about our study is that it shows that it’s never too late to quit. Some of the people in our study had smoked more than 15,000 packs of cigarettes over their life, but within a few years of quitting, many of the cells lining their airways showed no evidence of damage from tobacco,” he said. The comments appear in a press release issued by Cancer Research UK, which partly funded the study.

This study has “broadened our understanding of the effects of tobacco smoke on normal epithelial cells in the human lung,” Gerd P. Pfeifer, PhD, at the Center for Epigenetics, Van Andel Institute, Grand Rapids, Michigan, writes in an accompanying comment.

“It has shed light on how the protective effect of smoking cessation plays out at the molecular level in human lung tissue and raises many interesting questions worthy of future investigation,” he added.

‘Important public health message’

Joint senior author Sam M. Janes, PhD, Lungs for Living Research Center, UCL Respiratory, University College London, added that the study has “an important public health message.

“Stopping smoking at any age does not just slow the accumulation of further damage but could reawaken cells unharmed by past lifestyle choices,” he said.

“Further research into this process could help to understand how these cells protect against cancer and could potentially lead to new avenues of research into anticancer therapeutics,” Dr. James added.

In an interview, Dr. Campbell said that the team would next like to try “to find where this reservoir of normal cells hides out while the patient is smoking. We have some ideas from mouse models and we think, by adapting the methods we used in this study, we will be able to test that hypothesis directly.”

He continued: “If we can find this stem cell niche, then we can study the biology of the cells living in there and what makes them expand when a patient stops smoking.

“Once we understand that biology, we can think about therapies to target that population of cells in beneficial ways.”

Dr. Campbell concluded that they are “a long way away yet, but the toolkit exists for getting there.”

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