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Research reveals that non-smokers with non-small cell lung cancer 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.
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 in the journalIn the UK, lung cancer is the third most common type of cancer and the leading cause of cancer death.
Lung cancer treatments that target this mutation, known as EGFR inhibitors, have been available for over 15 years. However, while some patients see their cancer tumors shrink with EGFR inhibitors, other patients, particularly those with an additional mutation in the p53 gene , fail to respond and experience far worse survival rates. But scientists and clinicians have so far been unable to explain why this is the case.
The researchers then treated lung cancer cells in the lab, some with just the single EGFR mutation and some with both mutations, with an EGFR inhibitor. They found that within five weeks of exposure to the drug, a significantly higher percentage of cells with both the double mutation and double genomes had multiplied into new drug-resistant cells.
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