Study links DNA traits to risk level for smoking-related cancer
Jerusalem: A team of Israeli researchers has identified how the structure and chemical changes in the DNA influence the risk of developing lung cancer from smoking.
The team from the Hebrew University of Jerusalem focused on benzo(a)pyrene, a toxic chemical in cigarette smoke, which binds to DNA when processed by the body, disrupts its normal function, and causes damage to cells, Xinhua news agency reported.
The study, published in Nucleic Acids Research, found that the way DNA is organised and chemically altered can affect how smoking damages it, how well the body cells repair the damage, and how many mutations result from it.
It discovered that certain regions of DNA, particularly those that are more open and active, are more vulnerable to damage but also better at repairing themselves, and tend to have fewer mutations over time, whereas regions less efficiently repaired may accumulate mutations, increasing the risk of cancer.
The study also found that proteins regulating gene activity can sometimes protect DNA from harm, but in other cases, they can make it more vulnerable to damage, the researchers said.
The body's ability to repair DNA damage plays a more significant role in determining whether mutations occur, rather than just the amount of damage itself, they added. The study offers new insights into how smoking leads to lung cancer by damaging DNA and causing mutation and could help shape future strategies for cancer prevention and treatment.
According to the World Health Organisation (WHO), tobacco use accounts for 25 per cent of all cancer deaths globally and is the primary cause of lung cancer. It remains a public health issue of the utmost importance in the Region, where an estimated 186 million people (or 26 per cent of the adult population) currently use tobacco.
Smokers are up to 22 times more likely to develop lung cancer in their lifetime compared to non-smokers.
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