Title
The role of cMet in non-small cell lung cancer resistant to EGFR-inhibitors : did we really find the target?The role of cMet in non-small cell lung cancer resistant to EGFR-inhibitors : did we really find the target?
Author
Faculty/Department
Faculty of Medicine and Health Sciences
Research group
Molecular Imaging, Pathology, Radiotherapy & Oncology (MIPRO)
Publication type
article
Publication
Subject
Pharmacology. Therapy
Source (journal)
Current drug targets
Volume/pages
15(2014):14, p. 1284-1292
ISSN
1389-4501
ISI
000346421300004
Carrier
E
Target language
English (eng)
Full text (Publishers DOI)
Affiliation
University of Antwerp
Abstract
The advent of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) represented the most important innovation in NSCLC treatment over the last years. However, despite a great initial activity, secondary mutations in the same target, or different alterations in other molecular pathways, inevitably occur, leading to the emergence of acquired resistance, in median within the first year of treatment. In this scenario, the mesenchymal-epidermal transition (cMET) tyrosine kinase receptor and its natural ligand, the hepatocyte growth factor (HGF), seem to play an important role. Indeed either the overexpression or the amplification of cMET, as well as the overexpression of the HGF, have been reported in a substantial subgroup of NSCLC patients resistant to EGFR-TKIs. Several cMET-inhibitors have been developed as potential therapeutic candidates, and are currently under investigation in clinical trials. These compounds include both monoclonal antibodies and TKIs, and most of them have been investigated as dual combinations including an anti-EGFR TKI, to improve the efficacy of the available treatments, and ultimately overcome acquired resistance to EGFR-inhibitors.
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