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Acquired EGFR Mutation as the Potential Resistance Driver to Crizotinib in a MET- Mutated Tumor  Marc-Antoine Benderra, MD, Sandrine Aspeslagh, PhD, Sophie.

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Presentation on theme: "Acquired EGFR Mutation as the Potential Resistance Driver to Crizotinib in a MET- Mutated Tumor  Marc-Antoine Benderra, MD, Sandrine Aspeslagh, PhD, Sophie."— Presentation transcript:

1 Acquired EGFR Mutation as the Potential Resistance Driver to Crizotinib in a MET- Mutated Tumor 
Marc-Antoine Benderra, MD, Sandrine Aspeslagh, PhD, Sophie Postel-Vinay, PhD, Ludovic Bigot, MD, Thierry De Baere, PhD, Yohann Loriot, PhD, Ludovic Lacroix, PhD, Christophe Massard, PhD, Gilles Vassal, PhD, Fabrice André, PhD, Jean-Charles Soria, PhD  Journal of Thoracic Oncology  Volume 11, Issue 2, Pages e21-e23 (February 2016) DOI: /j.jtho Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions

2 Figure 1 Patient 1: clinical course, including treatment history and relevant imaging studies and tumor biopsy specimens. Representative images from computed tomography of the chest at different times: (A) at baseline (before administration of crizotinib), showing right pulmonary lesion; (B) at 3 months, with an excellent tumor response in right pulmonary lesion; and (C) at 10 months, with tumor progression. Abbreviations: DOC, docetaxel; EGFR, epidermal growth factor receptor; GEM, gemcitabine; KRAS, Kirsten rat sarcoma viral oncogene homolog; M, months; MIP, mitomycin-ifosfamide-cisplatin; NOTCHi, inhibitor of the Notch pathway; PAC-BEV, paclitaxel-bevacizumab; PEM, pemetrexed; WT, wild-type. Journal of Thoracic Oncology  , e21-e23DOI: ( /j.jtho ) Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions

3 Figure 2 Signaling pathways activated by hepatocyte growth factor and MET. Cytoplasmic effector molecules, including growth factor receptor-bound protein 2 (GRB2) and GRB2-associated binding protein (GAB1) are recruited to the docking site. Abbreviations: AKT, protein kinase B; ERK, extracellular signal-regulated kinase; HGF, hepatocyte growth factor; MAPK, mitogen-activated protein kinases; mTOR, mammalian target of rapamycine; NfkB, nuclear factor kappa B; PI3K, phosphatidyl inositol 3-OH-kinase; VEGFR, vascular endothelial growth factor receptor. Journal of Thoracic Oncology  , e21-e23DOI: ( /j.jtho ) Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions

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