Marie Fernandes

The paper shows that MET exon 14 skipping mutations eliminate the pro-apoptotic function of MET, converting it from a tumor suppressor to an oncogenic driver in lung adenocarcinomas.

The paper identifies a regulatory network involving ETS1, FOSL1, and SMAD3 that mediates MET exon 14 skipping in lung cancer, showing their role in RAS-ERK pathway activation and potential as therapeutic targets.

This paper identifies N-lobe MET mutations in HPRCC that require ligand stimulation for activation, unlike kinase domain mutations, and shows their sensitivity to MET inhibitors.