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Accueil Tracking MET de-addiction in lung cancer: A road towards the oncogenic target.
Tracking MET de-addiction in lung cancer: A road towards the oncogenic target. Imprimer Envoyer
Mardi, 29 Août 2017 07:18
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Tracking MET de-addiction in lung cancer: A road towards the oncogenic target.

Cancer Treat Rev. 2017 Aug 20;60:1-11

Authors: Pilotto S, Carbognin L, Karachaliou N, Ma PC, Rosell R, Tortora G, Bria E

Abstract
The discovery of druggable oncogenic drivers (i.e. EGFR and ALK), along with the introduction of comprehensive tumor genotyping techniques into the daily clinical practice define non-small-cell lung cancer (NSCLC) asa group of heterogeneous diseases, requiring a context-personalized clinico-therapeutical approach. Among the most investigated biomarkers, the MET proto-oncogene has been extensively demonstrated to play a crucial role throughout the lung oncogenesis, unbalancing the proliferation/apoptosis signaling and influencing the epithelial-mesenchymal transition and the invasive phenotype. Nevertheless, although different mechanisms eliciting the aberrant MET-associated oncogenic stimulus have been detected in lung cancer (such as gene amplification, increased gene copy number, mutations and MET/HGF overexpression), to date no clinically impactful results have been achieved with anti-MET tyrosine kinase inhibitors and monoclonal antibodies in the context of an unselected or MET enriched population. Recently, MET exon 14 splicing abnormalities have been identified asa potential oncogenic target in lung cancer, able to drive the activity of MET inhibitors in molecularly selected patients. In this paper, the major advancement and drawbacks of MET history in lung cancer are reviewed, underlying the renewed scientific euphoria related to the recent identification of MET exon 14 splicing variants asan actionable oncogenic target.

PMID: 28843992 [PubMed - as supplied by publisher]


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Accueil Tracking MET de-addiction in lung cancer: A road towards the oncogenic target. Top