Author of

• 30601

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  P2.01 - Advanced NSCLC (ID 159)

  • Event: WCLC 2019
  • Type: Poster Viewing in the Exhibit Hall
  • Track: Advanced NSCLC
  • Presentations: 1
  • Now Available
  • Moderators:
  • Coordinates: 9/09/2019, 10:15 - 18:15, Exhibit Hall

  • 30636

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    P2.01-35 - Acquired MET-Aberrance Is a Mechanism of Resistance to ALK Inhibitors in ALK-Positive Advanced Non-Small-Cell Lung Cancer     (Now Available) (ID 1739)

    10:15 - 18:15  |  Author(s): Han-Min Wang
    • Abstract
    • Slides

    Background
    

    Anaplastic lymphoma kinase tyrosine kinase inhibitor (ALK-TKI) is standard of care in ALK-positive advanced non-small-cell lung cancer (NSCLC). Unfortunately ALK-positive NSCLC patients treated with ALK TKIs inevitably develop resistance mediated by complex mechanisms including ALK mutations, ALK amplification, or activation of alternative signaling pathways. However, there are few reports about Mesenchymal-epithelial transition factor (MET) signal in NSCLC.

    Method
    

    Totally 136 ALK-positive advanced NSCLC patients were screened for ALK rearrangement detected by tumor tissue or plasma Next-generation sequencing(NGS) at the Guangdong Lung Cancer Institute from January 2016 to December 2018 .MET-aberrance was defined as c-Met overexpression performed by immunohistochemical(IHC) staining method with SP44 antibody and MET amplification assessed by tumor tissue or plasma Next-generation sequencing (NGS) or fluorescent in situ hybridization(FISH).

    Result
    

    Totally 5.89% (8/136) of patients were identified with MET-aberrance in 136 ALK-rearranged cases. Among the 8 patients，there were 6 with de novo MET-aberrance and 2 with acquired MET-aberrance.The median progression-free survival (PFS) in ALK-rearranged patients with de novo MET-aberrance was 9.6 months (95% CI 0.0 to 19.2months).The other 2 patients gained MET-aberrance after the treatment with alectinib. Both of them received lorlatinib, but the PFS only lasted for 2months. One achieved partial remission with crizotinib , which was originally developed as an inhibitor of the MET gene.

    Conclusion
    

    Acquired MET-aberrance maybe a mechanism of acquired resistance to the second-generation ALK-TKIs for ALK-rearranged advanced NSCLC patients.

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