Nature Communications (Jun 2016)

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

  • 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

DOI
https://doi.org/10.1038/ncomms11815
Journal volume & issue
Vol. 7, no. 1
pp. 1 – 15

Abstract

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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.