A team of Israeli researchers has identified how the structure and chemical modifications of 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 that, when processed by the body, binds to DNA, disrupts its normal function, and causes cellular damage, Xinhua News Agency reported.
Published in Nucleic Acids Research, the study found that DNA organization and chemical changes affect how smoking damages genetic material, how efficiently cells repair the damage, and how many mutations occur as a result.
The researchers discovered that certain DNA regions, particularly those that are more open and active, are more vulnerable to damage. However, these regions also demonstrate better repair mechanisms and accumulate fewer mutations over time. In contrast, regions with less efficient repair processes may accumulate mutations, increasing the risk of cancer.
The study also highlighted the role of proteins that regulate gene activity. While some proteins protect DNA from damage, others can make it more susceptible. The researchers emphasized that the body’s ability to repair DNA damage plays a greater role in determining mutation risk than the initial extent of damage itself.
These findings provide valuable insights into how smoking contributes to lung cancer by causing DNA damage and mutations. The research could help shape future cancer prevention and treatment strategies.
According to the World Health Organization (WHO), tobacco use accounts for 25% of all cancer-related deaths worldwide and is the leading cause of lung cancer. In the region, an estimated 186 million people (26% of the adult population) currently use tobacco, making it a major public health concern.
Smokers are up to 22 times more likely to develop lung cancer compared to non-smokers.
-IANS
