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Lung Cancer. 2016 Aug;98:59-61. doi: 10.1016/j.lungcan.2016.05.015. Epub 2016 May 25.

High MET amplification level as a resistance mechanism to osimertinib (AZD9291) in a patient that symptomatically responded to crizotinib treatment post-osimertinib progression.

Author information

  • 1Chao Family Comprehensive Cancer Center, University of California Irvine School of Medicine, Orange, CA 92868, USA. Electronic address: Ignatius.ou@uci.edu.
  • 2Foundation Medicine, Inc., Cambridge, MA 02141, USA.

Abstract

Third-generation EGFR TKI has been approved in the US and EU for the treatment of EGFR mutant T790M+ NSCLC patients that are resistant to first- or second generation EGFR TKIs. Here we report a patient who developed resistance to osimertinib after a confirmed partial response for 9 months. Pre-osimertinib and post-osimertinib tumor biopsy revealed the emergence of high level of MET amplification (30 copies) post osimertinib treatment. Patient was treated with single agent crizotinib, a known MET inhibitor, with transient symptomatic benefit. MET amplification is one potential resistance mechanism to osimertinib and combination of osimertinib and a MET inhibitor should be investigated post-osimertinib progression in EGFR mutant T790M+ NSCLC patients whose harbored acquired MET amplification.

KEYWORDS:

Acquired resistance; METamplification; Non-small-cell lung cancer; Osimertinib; Third-generation EGFR TKI

PMID:
27393507
DOI:
10.1016/j.lungcan.2016.05.015
[PubMed - in process]
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