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MET-EGFR dimerization in lung adenocarcinoma is dependent on EGFR mtations and altered by MET kinase

MET Addiction Can be Circumvented Through EGFR Inhibition Via AXL in MET-Amplified Primary ResistantEGFR-Mutant NSCLCX

Single targeting of MET in EGFR-mutated and MET-amplified non-small cell lung cancer

Combining EGFR and MET Inhibition With Crizotinib in EGFR-mutated Lung Adenocarcinoma Harboring MET Amplification

Outcome of EGFR-mutated NSCLC patients with MET-driven resistance to EGFR tyrosine kinase inhibitors

MET amplification increases the metastatic spread of EGFR-mutated NSCLC

Resistance mechanisms to dual EGFR and MET inhibition in patients with EGFR-mutant MET-amplified non-small

Dual MET/EGFR therapy leads to complete response and resistance prevention in a MET-amplified gastroesophageal

Expression of HGF, MET and mutated EGFR in EGFR mutated lung adenocarcinoma and their clinical significance

Impact of MET alterations on targeted therapy with EGFR-tyrosine kinase inhibitors for EGFR-mutant lung

MET inhibitors for targeted therapy of EGFR TKI-resistant lung cancer

Combinatorial approaches targeting the EGFR family and c-Met in SCCHN

Heat stress induced, ligand-independent MET and EGFR signalling in hepatocellular carcinoma

Expression level of EGFR and MET receptors regulates invasiveness of melanoma cells

Discovery of amivantamab (JNJ-61186372), a bispecific antibody targeting EGFR and MET

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