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We know that smoking cessation is an excellent way to lower your risk of lung cancer. So far, the experts were not sure why this was the case. Our latest research has shown that in people who quit smoking, the body actually fills the airways with normal, non-cancerous cells that help protect the lungs and reduce their risk of cancer.

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Cancer develops when a single villain cell takes on genetic changes called mutations that instruct that cell to ignore all normal growth restrictions, causing it to rapidly multiply out of control. Throughout our lives, all of our cells accept mutations at a constant rate about 20-50 mutations per cell and year. Fortunately, the vast majority of these mutations are completely harmless and do not affect our cells in any measurable way.

But occasionally a mutation in the wrong gene ends up in the wrong cell, driving the cell to cancer. We call these genetic changes driver mutations. For the cell to become a full-blown cancer cell, five to ten or more of these driver mutations are likely to be needed.

Thanks to advances in DNA sequencing technology, we are now able to examine all 3 billion DNA bases that make up the genetic blueprint of a cell (called the genome). By sequencing lung cancer cell DNA in smokers and non-smokers, we know that smoking increases the number of mutations.

The binding of tobacco carcinogens to DNA is affected by their chemical properties, which means that certain types of mutations occur more often than others. For tobacco, this leads to a clear signature of mutations that occur in the genome, which differs from other causes of DNA damage.

Our team was interested in the earliest stages of developing lung cancer. In particular, we try to understand what happens to normal cells when they are exposed to tobacco smoke.

To investigate this, we developed methods to isolate individual normal cells from small biopsies of a patients airways, and then grown these cells in an incubator to obtain enough DNA for sequencing. We then analyzed the genome of 632 cells from 16 study participants, including four non-smokers, six ex-smokers and three current smokers (all in middle age or older) and three children.

Among the never smokers, we found that the number of cell mutations increased with age. So when someone is 60 years old, every normal lung cell contains about 1,000 to 1,500 mutations. These mutations are caused by the normal wear and tear of life, the same type of mutation that we see in other organs in the body. Only about 5% of the cells of never-smokers were found to have driver mutations.

Also read: Early breast cancer treatment in India costs 10 years of average annual wages: WHO

With the current smokers, however, the picture was very different. We found that each lung cell had an average of 5,000 additional mutations that exceeded the expectations of a never-smoking age. It was even more striking that the variation from cell to cell also increased dramatically in smokers.

Some individual cells had 10,000-15,000 mutations ten times more mutations than we would have expected if the person had not smoked. These additional mutations had the signature that we would expect from the chemicals in tobacco smoke, which confirms that they can be traced directly to cigarettes.

In addition to an increase in the total number of mutations, there is also a significant increase in driver mutations. More than a quarter of the lung cells of all smokers currently examined had at least one drive mutation. Some even had two or three. Given that five to ten of these mutations can cause cancer, it is clear that many normal lung cells are likely to become cancerous in middle-aged or older smokers.

Our most exciting result was the people who quit smoking. We found that ex-smokers had two groups of cells. One group had the thousands of additional mutations seen in current smokers, but the other group was essentially normal. The normal cell group had the same number of mutations as we would expect in the cells from someone who had never smoked.

This nearly normal group of cells was four times larger in former smokers than in current smokers. This suggests that these cells increase to refill the airway lining after someone quits smoking. We have seen this expansion of nearly normal cells in former smokers who have smoked a pack of cigarettes daily for more than 40 years.

The reason why this finding is so exciting is that this almost normal group of cells protects against cancer. When we examine a former smokers lung cancer cell, it always comes from the badly damaged group of cells not from the almost normal group.

Now we know why our risk of cancer decreases so much because the body fills the airways with cells that are essentially normal. The next step will be to find out how this group of cells manages to avoid damage from cigarette smoke and how we can encourage them to recover even more.

One possible explanation which emerges from previous work on mouse models is that a group of stem cells is buried deep in the glands that produce the mucus secreted from the airways. This place would of course be better protected from tobacco smoke than the surface of the airways.

Our research is currently repeating that quitting smoking at any age not only slows the accumulation of further damage, but also wakes up cells that were not damaged by previous lifestyle choices.

Sam Janes, Professor of Respiratory Medicine, UCL and Peter Campbell, Head of Cancer, Aging and Somatic Mutation, Wellcome Trust Sanger Institute

This article was republished in The Conversation under a Creative Commons license. Read the original article.

Also read: One in 15 Indians will die from cancer, the WHO report says

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New research shows what happens to your lung cells once you quit smoking - Daily Gaming Worlld