MET Alterations
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Understand the importance of biomarkers in the management of your patients with NSCLC


The impact of MET alterations in your patients with NSCLC…


of patients like yours may have an oncogenic MET alteration1,2


of patients like yours may have an oncogenic METex14 skipping


of patients like yours may have a high-level oncogenic METamp alteration1,2

The MET protein is key to normal processes – but it is susceptible to dysregulation1,3,4

Studies show that the MET pathway is critical for normal biologic processes, including embryonic and organ development, tissue repair and wound healing.1,3,4


Dysregulation of the MET pathway can occur through many mechanisms, including:1,3,4

  • - exon 14 skipping
  • - amplification
  • - rearrangement
  • - fusion
  • - activating mutations in the kinase domain


With MET receptor overexpression observed in 35–72% of NSCLC tumors.1

The MET pathway is key for normal biological processes including cell motility, proliferation and apoptosis regulation3

Up to 6% of your patients with NSCLC may harbor MET alterations responsible for driving oncogenesis

MET alterations (namely, METex14 skipping and METamp) occur in up to 6% of patients with NSCLC, and correlate independently with advanced disease stage.3,4 3–4% of patients like yours with NSCLC may harbor a METex14 skipping alteration, correlating with a poorer

prognosis.1,2,5,6 The presence of METex14 skipping is mutually exclusive to commonly tested oncogenic drivers, such as RET, BRAF, ALK, EGFR and ROS1.7,8 

METex14 and METamp alterations could be present in up to 6% of your NSCLC patients

Approximately 79% of patients with NSCLC adenocarcinoma may have an oncogenic driver alteration, including up to 6% who may have MET alterations. The remaining 21% are estimated to be wild type for the main known oncogenic drivers


*Prevalence of gene mutations varies between studies

METex14 and METamp can both contribute to oncogenic potential12

Oncogenic MET alterations cause aberrant activation of the MET pathway, driving tumor growth and are associated with acquired resistance.3,4,11 


  • • Loss of MET exon 14 through exon skipping leads to increased MET stability and sustained signaling upon hepatocyte growth factor stimulation11 
  • METamp results in an increased copy number of the MET gene, and has been implicated as one of the major mechanisms driving EGFR TKI resistance, through the activation of downstream pathways and providing a bypass pathway for EGFR TKIs5,11  
  • • Both METex14 and METamp promote tumor proliferation, invasive growth, metastatic spread and anti-apoptosis11

Your patients with MET-altered NSCLC could face aggressive disease and poor prognosis12

Patients with NSCLC harboring MET alterations have a higher association with advanced stage disease.7 A multivariate survival analysis assessing overall survival in patients with METex14 patients (n=18) or METamp (n=8) NSCLC demonstrated that those with either of these alterations had a significantly shorter OS compared to those without.12

References and Abbreviations

Expand all Collapse all

OS, overall survival

*Approximate prevalence


1. Salgia R. Mol Cancer Ther 2017; 16:555–565. 

2. Ikeda S et al. J Hematol Oncol 2018; 11:76. 

3. Drilon A et al. J Thorac Oncol 2017; 12:15–26.

4. Wu YL et al. Cancer Treat Rev 2017; 61:70–81.

5. Wang Q et al. J Hematol Oncol 2019; 12:63.

6. Sterlacci W et al. Virchows Arch 2017; 471:49–55.

7. Awad MM et al. Lung Cancer 2019; 133:96–102. 

8. Frampton GM et al. Cancer Discov 2015; 5:850–859.

9. Pakkala S, Ramalingam SS. JCI Insight 2018; 3:e120858. 

10. Rossell R, Karachaliou N. Lancet 2016; 387:1354–1356. 

11. Kim EK et al. Clin Lung Cancer 2019; 20:e123–32. 

12. Tong JH et al. Clin Cancer Res 2016; 22:3048–3056. 

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