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Abnormal activation of mesenchymal epithelial transition (MET) receptor tyrosine kinase is associated with oncogenesis. Various underlying mechanisms, including alteration, amplification, gene rearrangement, and exon skipping in the transcript account for abnormal MET signaling. One of the critical alterations in MET leading to non-small cell lung carcinoma (NSCLC) is MET exon 14 (METex14) skipping, a driver mutation, which accounts for approximately 3–4% of lung adenocarcinoma. METex14 skipping results in the formation of a functionally active and stable truncated receptor lacking the juxtamembrane regulatory domain responsible for MET ubiquitination. Several MET kinase inhibitors have been developed targeting MET receptors, and many are in clinical trials. The US Food and Drug Administration has recently approved capmatinib (Tabrecta; Novartis, Basel, Switzerland) for the treatment of NSCLC with METex14 skipping alteration. We review the current understanding of the implications of aberrant MET activation in NSCLC harboring METex14 skipping alteration, available diagnostic options, potential therapies in the pipeline, and the future clinical landscape for such alterations.

MET Exon 14 Skipping Alterations in Non-small Cell Lung Carcinoma—Current Understanding and Therapeutic Advances