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Title: | Responses to Crizotinib Can Occur in High-Level MET-Amplified Non-Small Cell Lung Cancer Independent of MET Exon 14 Alterations |
Authors: | CAPARICA, Rafael; YEN, Cheng Tzu; COUDRY, Renata; IGNATIUS, Sai-Hong; VARELLA-GARCIA, Marileila; CAMIDGE, D. Ross; CASTRO JR., Gilberto de |
Citation: | JOURNAL OF THORACIC ONCOLOGY, v.12, n.1, p.141-144, 2017 |
Abstract: | Activation of the MET proto-oncogene (MET) highly sensitive to MET inhibition has recently been described in NSCLC through two mechanisms: high-level amplification of the MNNG HOS Transforming gene (MET) (usually expressed relative to the chromosome 7 centromere [CEP7] when using fluorescence in situ hybridization) and exon 14 alterations. As partial overlap of these biomarkers occurs, whether one is purely a surrogate for the other or both can represent true oncogenic driver states continues to be explored. Cases of MET inhibitor-sensitive NSCLC harboring exon 14 alterations without coincident amplification have already been described. Here we report two cases of MET inhibitor-sensitive NSCLC harboring high-level MET amplification (MET/CEP7 ratio >= 5) without coincident exon 14 alterations, suggesting that these two methods of MET activation can produce independent MET-addicted states in NSCLC. Molecular profiling designed to capture all cases of potentially MET-addicted NSCLC should address both activation mechanisms. |
Appears in Collections: | Artigos e Materiais de Revistas Científicas - HC/ICESP Artigos e Materiais de Revistas Científicas - HC/InRad Artigos e Materiais de Revistas Científicas - LIM/24 Artigos e Materiais de Revistas Científicas - ODS/03 |
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