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dc.contributor.authorCalifano, Raffaele
dc.contributor.authorMorgillo, F
dc.contributor.authorDe Mello, R
dc.contributor.authorMountzios, G
dc.date.accessioned2015-07-01T07:50:34Zen
dc.date.available2015-07-01T07:50:34Zen
dc.date.issued2015-04en
dc.identifier.citationRole of mesenchymal-epithelial transition amplification in resistance to anti-epidermal growth factor receptor agents. 2015, 3 (6):81 Ann Transl Meden
dc.identifier.issn2305-5839en
dc.identifier.pmid25992380en
dc.identifier.doi10.3978/j.issn.2305-5839.2015.03.44en
dc.identifier.urihttp://hdl.handle.net/10541/558717en
dc.description.abstractAll patients with epidermal growth factor receptor (EGFR) mutant advanced non-small cell lung cancer (NSCLC) treated with an EGFR-tyrosine kinase inhibitor (EGFR-TKI) such as gefitinib, erlotinib or afatinib will progress after a median of 9-12 months. So far, development of a secondary T790M mutation represents the most common (approximately 60%) mechanism of resistance to these drugs. The relative rarity of mesenchymal-epithelial transition (MET) amplification in NSCLC suggests that this event plays a limited role in primary resistance to EGFR-TKI. In contrast, MET gene amplification has been detected as a secondary event representing one of the most relevant mechanisms involved in the acquired resistance to EGFR-TKIs both in preclinical and clinical studies. The aim of this review is to discuss the role of MET amplification as a mechanism of resistance to anti-EGFR therapies and to review strategies which aim at overcoming this mechanism of resistance, including studies assessing drug combinations targeting both EGFR and MET pathways.
dc.language.isoenen
dc.rightsArchived with thanks to Annals of translational medicineen
dc.titleRole of mesenchymal-epithelial transition amplification in resistance to anti-epidermal growth factor receptor agents.en
dc.typeArticleen
dc.contributor.departmentCancer Research UK Department of Medical Oncology, The Christie NHS Foundation Trust, Manchester M20 4BXen
dc.identifier.journalAnnals of Translational Medicineen
html.description.abstractAll patients with epidermal growth factor receptor (EGFR) mutant advanced non-small cell lung cancer (NSCLC) treated with an EGFR-tyrosine kinase inhibitor (EGFR-TKI) such as gefitinib, erlotinib or afatinib will progress after a median of 9-12 months. So far, development of a secondary T790M mutation represents the most common (approximately 60%) mechanism of resistance to these drugs. The relative rarity of mesenchymal-epithelial transition (MET) amplification in NSCLC suggests that this event plays a limited role in primary resistance to EGFR-TKI. In contrast, MET gene amplification has been detected as a secondary event representing one of the most relevant mechanisms involved in the acquired resistance to EGFR-TKIs both in preclinical and clinical studies. The aim of this review is to discuss the role of MET amplification as a mechanism of resistance to anti-EGFR therapies and to review strategies which aim at overcoming this mechanism of resistance, including studies assessing drug combinations targeting both EGFR and MET pathways.


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