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Case report: HER2 amplification as a resistance mechanism to crizotinib in NSCLC with MET exon 14 skipping

Guanggui Ding1, Jian Wang1, Peikun Ding1

  • 1a Department of Thoracic Surgery , Shenzhen People's Hospital, Second Clinical Medical College of Jinan University.

Cancer Biology & Therapy
|February 13, 2019
PubMed

Insights

Crizotinib effectively treats non-small cell lung cancer (NSCLC) with MET exon 14 skipping. However, HER2 amplification emerged as a novel resistance mechanism, highlighting bypass pathways in acquired resistance to MET inhibitors.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Non-small cell lung cancer (NSCLC) patients with MET exon 14 skipping mutations often respond to crizotinib.
  • Established resistance mechanisms include MET D1228N and Y1230C mutations.

Observation:

  • A Chinese NSCLC patient with MET exon 14 skipping achieved remission with crizotinib.
  • Disease progression occurred, revealing amplification of multiple genes, including erb-b2 receptor tyrosine kinase 2 (HER2).

Findings:

  • This case represents the first report of HER2 gene amplification in an NSCLC patient with MET exon 14 skipping during crizotinib treatment.
  • The findings suggest that bypass mechanisms, such as HER2 amplification, contribute to acquired resistance against MET inhibitors.

Implications:

  • Understanding novel resistance mechanisms like HER2 amplification is crucial for developing effective treatment strategies for NSCLC.
  • This highlights the need for continuous monitoring and adaptive therapies in patients treated with MET inhibitors.
Keywords:
HER2 amplificationMET 14 skippingNGSNSCLCcrizotinibresistancetargeted therapy

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