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Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
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MET Y1003S point mutation shows sensitivity to crizotinib in a patient with lung adenocarcinoma

Yun L Miao1, Qing Qing Xu1

  • 1The Affiliated Drum Tower Hospital of Medical College of Nanjing University, No. 321, Zhongshan Road, 210000 Nanjing, China.

Lung Cancer (Amsterdam, Netherlands)
|March 20, 2019
PubMed
Abstract

Insights

A MET Y1003S mutation in lung adenocarcinoma responded well to crizotinib treatment, showing tumor remission. This finding highlights crizotinib as a potential therapy for MET-altered non-small cell lung cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • MET amplification and MET exon 14 skipping mutations are known targets for crizotinib in non-small cell lung cancer (NSCLC).
  • The Y1003 binding site is crucial for MET protein degradation via E3 ubiquitin ligase.
  • Understanding novel MET mutations is key to expanding targeted therapy options for NSCLC.

Observation:

  • A never-smoking 61-year-old female presented with advanced adenocarcinoma and enlarged lymph nodes.
  • Cell-free circulating tumor DNA (ctDNA) analysis revealed a MET Y1003S mutation.
  • This mutation was functionally predicted to be similar to MET exon 14 skipping mutations.

Findings:

  • The patient received crizotinib, a MET and ALK inhibitor.
  • Dramatic tumor remission was observed within one month, lasting over ten months.
  • CT scans confirmed significant reduction in lung and lymph node lesions, meeting partial response criteria.

Implications:

  • MET Y1003 alterations represent a diverse group of mutations sensitive to MET inhibitors.
  • This case supports crizotinib's efficacy in NSCLC patients with MET Y1003S mutations.
  • Targeted inhibition of MET offers a promising therapeutic strategy for specific NSCLC subtypes.
Keywords:
CrizotinibMETMET inhibitorMutationNon-small cell lung cancerY1003

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