Circulating tumour DNA profiling reveals heterogeneity of EGFR inhibitor resistance mechanisms in lung cancer patients

Circulating tumour DNA profiling reveals heterogeneity of EGFR inhibitor resistance mechanisms in lung cancer patients

EGFR-mutant non-small cell lung cancer is routinely treated with EGFR inhibitors, although resistance inevitably develops. Here, the authors sequence circulating tumour DNA and show that resistance to the third-generation inhibitor rociletinib is heterogeneous and recurrently involves somatic altera...

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Autores principales: Jacob J. Chabon, Andrew D. Simmons, Alexander F. Lovejoy, Mohammad S. Esfahani, Aaron M. Newman, Henry J. Haringsma, David M. Kurtz, Henning Stehr, Florian Scherer, Chris A. Karlovich, Thomas C. Harding, Kathleen A. Durkin, Gregory A. Otterson, W. Thomas Purcell, D. Ross Camidge, Jonathan W. Goldman, Lecia V. Sequist, Zofia Piotrowska, Heather A. Wakelee, Joel W. Neal, Ash A. Alizadeh, Maximilian Diehn
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2016
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Science
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Acceso en línea:https://doaj.org/article/e467721976a7414699480c405cfa9845
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Sumario:EGFR-mutant non-small cell lung cancer is routinely treated with EGFR inhibitors, although resistance inevitably develops. Here, the authors sequence circulating tumour DNA and show that resistance to the third-generation inhibitor rociletinib is heterogeneous and recurrently involves somatic alterations of MET, EGFR, PIK3CA, ERRB2, and KRAS.

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