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• W2035204920 abstract "Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), such as gefitinib and erlotinib, are the first targeted therapy drugs approved for the treatment of advanced non-small-cell lung cancer (NSCLC). Interestingly, treatment with these small molecule, reversible EGFR-TKIs leads to more positive response rates in patients with adenocarcinoma, in females, Asians, and patients with no history of smoking. Positive responses to treatment in these populations may be due to the increased prevalence of mutations in the EGFR gene. Several distinct mutations in the EGFR gene have been identified in specimens from patients with NSCLC who responded to treatment with anilinoquinazoline EGFR inhibitors. However, despite the dramatic initial response to TKIs, most lung cancer patients relapse and subsequently become resistant to the drug, a process termed acquired resistance. The precise mechanisms underlying acquired resistance remain unclear. Resistance to EGFR-TKIs could result from several potential mechanisms, including development of a secondary mutation in EGFR (such as T790M), amplification of the MET receptor tyrosine kinase gene, or overexpression of other receptor tyrosine kinases." @default.
• W2035204920 created "2016-06-24" @default.
• W2035204920 creator A5065380119 @default.
• W2035204920 creator A5072556453 @default.
• W2035204920 creator A5082857859 @default.
• W2035204920 creator A5085340844 @default.
• W2035204920 date "2010-04-15" @default.
• W2035204920 modified "2023-10-10" @default.
• W2035204920 title "Acquired resistance of lung adenocarcinoma to EGFR-tyrosine kinase inhibitors gefitinib and erlotinib" @default.
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• W2035204920 doi "https://doi.org/10.4161/cbt.9.8.11881" @default.
• W2035204920 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20404520" @default.
• W2035204920 hasPublicationYear "2010" @default.
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