Respiratory Medicine Case Reports (Jan 2017)

Successful crizotinib monotherapy in EGFR-mutant lung adenocarcinoma with acquired MET amplification after erlotinib therapy

  • Katsuhiro Yoshimura, MD,
  • Naoki Inui, MD, PhD,
  • Masato Karayama, MD, PhD,
  • Yusuke Inoue, MD,
  • Noriyuki Enomoto, MD, PhD,
  • Tomoyuki Fujisawa, MD, PhD,
  • Yutaro Nakamura, MD, PhD,
  • Kengo Takeuchi, MD, PhD,
  • Haruhiko Sugimura, MD, PhD,
  • Takafumi Suda, MD, PhD

DOI
https://doi.org/10.1016/j.rmcr.2017.02.009
Journal volume & issue
Vol. 20, no. C
pp. 160 – 163

Abstract

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MET is a driver oncogene in non-small-cell lung cancer (NSCLC), and its amplification is associated with acquired resistance to epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors. A 56-year-old Japanese male with lung adenocarcinoma harboring an EGFR exon 21 L858R mutation received erlotinib to which he responded for 12 months. After disease progression, re-biopsy analyses revealed newly developed MET amplification. Neither EGFR exon 20 T790M mutation nor MET exon 14 mutations were detected. The MET inhibitor, crizotinib, showed a dramatic response. This is the first report of successful crizotinib single-agent therapy in EGFR-mutant NSCLC that acquired MET amplification during erlotinib therapy.

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