Table 1.

Reported incidence and functional consequences of MET biomarkers in lung cancer

MET dysregulationFunctional consequencesBiomarkerReported incidence in samples from lung cancer patientsReference
Gene overexpressionReduces or removes the requirement for ligand activation, leading to sustained or altered signaling properties of the receptorMET/p-MET expression by IHCNSCLC
37% IHC ≥2+(36)
61% IHC ≥2+(37)
ADC
35%(76)
67% IHC ≥2+(37)
72%(77)
SCC
38%(77)
p-MET in NSCLC
67%(35, 37)
HGF expressionLigand-induced activation could cause sustained or altered signalingCirculating plasma HGFElevated in SCLC(40)
Gene mutationMET mutation can lead to reduced degradation, with consequent overexpression and sustained or altered signalingMET exon 14 skipping mutationADC
3%(43–46)
4%(43, 44, 46, 78)
SCC
2%(45)
Other lung cancer subtypes
2%(43, 44, 46)
1%–8%(45)
Gene amplificationCan lead to overexpression and reduce or remove the requirement for ligand activation, leading to sustained or altered signaling properties of the MET receptorMET GCNNewly diagnosed ADC
MET/CEP7 ratio2%(46)
4%(21, 56)
5%(55)
EGFR TKI-resistant ADC
5%(57, 58)
17%(33)
21%(31)
22%(34)
Gene rearrangementMay reduce or remove the requirement for ligand activation, leading to sustained or altered signaling properties of the MET receptorMET rearrangementIdentified in an ADC patient(67)
Downstream MET signaling alterationDecreases RTK turnover to perpetuate oncogenic activation of METCBL mutation or LOHDetected in NSCLC patients(69)
  • Abbreviations: ADC, adenocarcinoma; CEP, chromosome enumeration probe; SCC, squamous cell carcinoma.