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- W2899679902 endingPage "652" @default.
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- W2899679902 abstract "While the development of EGFR-targeted tyrosine kinase inhibitors (TKIs) has revolutionized treatment of EGFR mutation-positive non-small-cell lung cancer, acquired resistance to therapy is inevitable, reflecting tumor evolution. Recent studies show that EGFR mutation-positive non-small-cell lung cancer is highly heterogeneous at the cellular level, facilitating clonal expansion of resistant tumors via multiple molecular mechanisms. Here, we review the mechanistic differences between first-, second- and third-generation EGFR-targeted TKIs and speculate how these features could explain differences in clinical activity between these agents from a clonal evolution perspective. We hypothesize that the molecular dissection of tumor resistance mechanisms will facilitate optimal sequential use of EGFR TKIs in individual patients, thus maximizing the duration of chemotherapy-free treatment and survival benefit." @default.
- W2899679902 created "2018-11-16" @default.
- W2899679902 creator A5007143858 @default.
- W2899679902 creator A5055160098 @default.
- W2899679902 creator A5056893617 @default.
- W2899679902 creator A5070801716 @default.
- W2899679902 date "2019-02-01" @default.
- W2899679902 modified "2023-10-18" @default.
- W2899679902 title "Tumor clonality and resistance mechanisms in <i>EGFR</i> mutation-positive non-small-cell lung cancer: implications for therapeutic sequencing" @default.
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- W2899679902 doi "https://doi.org/10.2217/fon-2018-0736" @default.
- W2899679902 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30404555" @default.
- W2899679902 hasPublicationYear "2019" @default.
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