MET Gene Status in Malignant Mesothelioma Using Fluorescent In Situ Hybridization Serena Varesano, PhD, Sandra Salvi, PhD, Simona Boccardo, PhD, Jean.

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MET Gene Status in Malignant Mesothelioma Using Fluorescent In Situ Hybridization Serena Varesano, PhD, Sandra Salvi, PhD, Simona Boccardo, PhD, Jean Louis Ravetti, MD Journal of Thoracic Oncology Volume 11, Issue 2, Pages e28-e30 (February 2016) DOI: 10.1016/j.jtho.2015.10.019 Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions

Figure 1 Patterns of MET gene status in malignant mesothelioma (MM). The frequency of MET gene status (i.e., amplified, polysomic, or disomic) seen in our study is indicated on the left. (A and B) One case of epithelioid mesothelioma with MET gene amplification and high expression of MET protein, respectively. (D and E) One case of epithelioid MM with MET gene polysomy and low expression of MET protein, respectively. (G and H) One case of epithelioid MM with MET gene disomy and negative expression of MET protein, respectively. (A, D, and G) Fluorescence in situ hybridization (FISH) for MET gene (original magnification, ×100). MET gene amplification was investigated using FISH with a MET/CEP7 probe cocktail (Vysis MET Spectrum Red FISH Probe Kit reagent/Vysis CEP 7 [D7Z1] SpectrumGreen Probe, both reagents from Abbott Molecular, Des Plaines, IL). White arrows indicate spots of MET red signal points. (B, E, and H) Immunohistochemistry (IHC) for MET protein (original magnification, ×40). IHC staining of MET was performed using Anti-c-Met Antibody IHC-plus LS-B2812 (LSBio, Seattle, WA). Black arrows indicate membrane and cytoplasmic positive staining. (C, F, and I) Hematoxylin–eosin stain (original magnification, ×10). Journal of Thoracic Oncology 2016 11, e28-e30DOI: (10.1016/j.jtho.2015.10.019) Copyright © 2015 International Association for the Study of Lung Cancer Terms and Conditions