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e-Poster Display Session

4P - Prevalence of MET Exon 14-mutations or MET amplification in non-small cell lung cancer in Swiss patients


24 Mar 2021


e-Poster Display Session


Spasenija Savic Prince


Journal of Thoracic Oncology (2021) 16 (suppl_4): S699-S703.


S. Savic Prince1, M. Bihl2, S. Eppenberger-Castori2, M.S. Matter2, N. Zellweger2, S.I. Rothschild2, L. Bubendorf3

Author affiliations

  • 1 University Hospital Basel, Basel/CH
  • 2 University Hospital Basel, 4031 - Basel/CH
  • 3 University Hospital Basel - Institute of Pathology, 4031 - Basel/CH

Abstract 4P


MET-targeted treatment has improved by the introduction of highly selective MET inhibitors for advanced stage MET Exon 14-mutated or MET-amplified non-small cell lung cancer (NSCLC). MET exon 14 skipping mutations occur in 3% and MET amplification in 1 to 6% of unselected NSCLC. The aim of our study was to investigate the prevalence of these MET alterations in treatment-naïve pre-selected NSCLC from our routine clinical practice, were MET analyses were generally performed sequentially in NSCLC with high MET expression and wild type status for EGFR, KRAS, ALK and ROS1.


580 consecutive treatment-naïve NSCLC who underwent routine predictive testing were retrospectively evaluated. High MET expression, as determined by immunohistochemistry (IHC), was defined as complete membranous MET staining with at least moderate intensity in ≥50% of tumor cells. MET exon 14 analysis was performed by Sanger sequencing. MET gene copy numbers were evaluated by fluorescence in situ hybridization (FISH) and MET amplification was defined as a MET/CEN7 ratio of ≥2.0. MET IHC was performed on histology specimens and cellblocks, but not on conventional cytology preparations. Therefore, prevalence data of MET alterations were analyzed separately for IHC pre-selected and non-preselected NSCLC wild type for other oncogenic driver alterations.


66% (302/457) of NSCLC had high MET expression. There was no difference between the prevalence of MET exon 14 mutations in IHC pre-selected and non-preselected NSCLC wild type for other oncogenic driver alterations (8.3% (9/108) and 8.1% (7/86), respectively, p = 1.0). In contrast, the prevalence of MET amplification was higher in MET IHC pre-selected NSCLC (11.5% (11/96) and 3.2% (1/31), respectively, p = 0.29).


MET exon14 skipping mutations are enriched in NSCLC wild type for other oncogenic driver alterations with the prevalence of >8% being higher compared to the published literature in unselected NSCLC (3%). High MET expression does not enrich for MET exon 14 mutations. However, MET IHC seems to be a cost-effective approach for pre-screening NSCLC for further MET FISH analysis.

Legal entity responsible for the study

The authors.


Has not received any funding.


S. Savic Prince: Honoraria (self), Advisory/Consultancy: Pfizer; Honoraria (self): Roche; Honoraria (self), Advisory/Consultancy: AstraZeneca. S.I. Rothschild: Advisory/Consultancy, Research grant/Funding (self): AstraZeneca; Advisory/Consultancy: Pfizer; Advisory/Consultancy: Takeda; Advisory/Consultancy: MSD Oncology; Advisory/Consultancy: Novartis; Advisory/Consultancy, Research grant/Funding (self): Boerhinger-Ingelheim; Advisory/Consultancy: Bristol-Myers Squibb; Advisory/Consultancy: Eli Lilly; Advisory/Consultancy: Eisai; Advisory/Consultancy, Research grant/Funding (self): Meck Serono; Research grant/Funding (self): AbbVie; Advisory/Consultancy: Amgen; Advisory/Consultancy: PharmaMar; Advisory/Consultancy, Research grant/Funding (institution): Roche. L. Bubendorf: Honoraria (self), Advisory/Consultancy: Pfizer; Advisory/Consultancy, Research grant/Funding (institution): Roche. All other authors have declared no conflicts of interest.

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