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    Role of mesenchymal-epithelial transition amplification in resistance to anti-epidermal growth factor receptor agents.

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    Authors
    Califano, Raffaele
    Morgillo, F
    De Mello, R
    Mountzios, G
    Affiliation
    Cancer Research UK Department of Medical Oncology, The Christie NHS Foundation Trust, Manchester M20 4BX
    Issue Date
    2015-04
    
    Metadata
    Show full item record
    Abstract
    All 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.
    Citation
    Role of mesenchymal-epithelial transition amplification in resistance to anti-epidermal growth factor receptor agents. 2015, 3 (6):81 Ann Transl Med
    Journal
    Annals of Translational Medicine
    URI
    http://hdl.handle.net/10541/558717
    DOI
    10.3978/j.issn.2305-5839.2015.03.44
    PubMed ID
    25992380
    Type
    Article
    Language
    en
    ISSN
    2305-5839
    ae974a485f413a2113503eed53cd6c53
    10.3978/j.issn.2305-5839.2015.03.44
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