Research reveals that non-smokers with non-small cell lung cancer (NSCLC) often resist targeted treatments due to mutations in the EGFR and p53 genes, which lead to genome doubling and drug resistance. This has significant implications for treatment strategies and diagnostic tests. Researchers have discovered the reason why targeted treatment for non-small cell lung cancer fails to work for some patients, particularly those who have never smoked.
The study shows that lung cancer cells with two particular genetic mutations are more likely to double their genome, which helps them to withstand treatment and develop resistance to it. Conducted by researchers from UCL, the Francis Crick Institute, and AstraZeneca, the study is published today (June 13) in the journal Nature Communications . Epidemiology and Genetic Factors of NSCLC In the UK, lung cancer is the third most common type of cancer and the leading cause of cancer death.
Around 85% of patients with lung cancer have non-small cell lung cancer (NSCLC), and this is the most common type found in patients who have never smoked. Considered separately, ‘never smoked’ lung cancer is the fifth most common cause of cancer death in the world. The most common genetic mutation found in NSCLC is in the epidermal growth factor receptor gene (EGFR), which enables cancer cells to grow faster.
It is found in about 10-15% of NSCLC cases in the UK, particularly in patients who have never smoked. Challenges of Current Treatments Surviva.
