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

•MET amplification as resistance to osimertinib.•Crizotinib provided temporary symptom relief.•Combination of Osiemrtinib+MET inhibitor should be investigated. 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 fi...

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Bibliographic Details
Published in:Lung cancer (Amsterdam, Netherlands) Netherlands), 2016-08, Vol.98, p.59-61
Main Authors: Ou, Sai-Hong Ignatius, Agarwal, Nikita, Ali, Siraj M.
Format: Article
Language:English
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Summary:•MET amplification as resistance to osimertinib.•Crizotinib provided temporary symptom relief.•Combination of Osiemrtinib+MET inhibitor should be investigated. 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.
ISSN:0169-5002
1872-8332
DOI:10.1016/j.lungcan.2016.05.015