sábado, 9 de enero de 2016

Response to crizotinib observed in lung adenocarcinoma with MET copy number gain but without high-level MET/CEP7 ratio, MET overexpression or exon 14 splicing mutations.

 2015 Dec 24. pii: S1556-0864(15)00255-5. doi: 10.1016/j.jtho.2015.12.102. [Epub ahead of print]

Response to crizotinib observed in lung adenocarcinoma with MET copy number gain but without high-level MET/CEP7 ratio, MET overexpression or exon 14 splicing mutations.

Zhang Y1Wang W2Wang Y1Xu Y1Tian Y3Huang M4Lu Y1.

Abstract

Mesenchymal-epithelial transition (MET) is an important driver gene in non-small cell lung cancer (NSCLC). Yet, MET-relevant biomarkers to predictive clinical response of MET inhibitors remain elusive. Limited studies indicated some possibly effective biomarkers including amplification with high-level MET/CEP7 ratio, MET exon 14 (METex14) splicing mutations and overexpression. MET copy number gain (MCNG) is an independent negative prognostic factor in NSCLC. Therefore, whether or not MCNG as a predictive biomarker to MET inhibitors remains lack of clinical evidence. Here we report a lung adenocarcinoma patient with MCNG but without high-level MET/CEP7 ratio or METex14 splicing mutations who achieved a rapid response to crizotinib, indicating MCNG may be an independent predictive biomarker to MET inhibitors.
Copyright © 2015 International Association for the Study of Lung Cancer. Published by Elsevier Inc. All rights reserved.

KEYWORDS:

MET/CEP7 ratio; Mesenchymal-epithelial transition; copy number gain; crizotinib; lung cancer
PMID:
 
26724472
 
[PubMed - as supplied by publisher]

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