MET overexpression and gene amplification in NSCLC: a clinical perspective

Lorenza Landi, Gabriele Minuti, Armida D'Incecco, Jessica Salvini, Federico CappuzzoMedical Oncology Department, Istituto Toscano Tumori, Ospedale Civile, Livorno, ItalyAbstract: The transmembrane tyrosine kinase mesenchymal-epidermal transition (MET) receptor and its ligand, hepatocyte grow...

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Autores principales:	Landi L, Minuti G, D&#39;Incecco A, Salvini J, Cappuzzo F
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2013
Materias:	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
Acceso en línea:	https://doaj.org/article/22c9f43c6aca43b68b29d128428afaee
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spelling	oai:doaj.org-article:22c9f43c6aca43b68b29d128428afaee2021-12-02T01:20:53ZMET overexpression and gene amplification in NSCLC: a clinical perspective1179-2728https://doaj.org/article/22c9f43c6aca43b68b29d128428afaee2013-06-01T00:00:00Zhttp://www.dovepress.com/met-overexpression-and-gene-amplification-in-nsclc-a-clinical-perspect-a13401https://doaj.org/toc/1179-2728Lorenza Landi, Gabriele Minuti, Armida D'Incecco, Jessica Salvini, Federico CappuzzoMedical Oncology Department, Istituto Toscano Tumori, Ospedale Civile, Livorno, ItalyAbstract: The transmembrane tyrosine kinase mesenchymal-epidermal transition (MET) receptor and its ligand, hepatocyte growth factor, also known as scatter factor, have recently been identified as novel promising targets in several human malignancies, including non-small cell lung cancer (NSCLC). Amplification, mutation, or overexpression of the MET gene can result in aberrant activation of the MET axis, leading to migration, invasion, proliferation, metastasis, and neoangiogenesis of cancer cells, suggesting that interfering with the MET/hepatocyte growth factor pathway could represent a potential antitumor strategy. While the role of MET mutations in NSCLC is not as yet fully understood, retrospective studies have shown that an increased MET gene copy number is a negative prognostic factor. In NSCLC, amplification of the MET gene is a relatively rare event, occurring in approximately 4% of patients not previously exposed to systemic therapies and in up to 20% of patients with acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors. In preclinical models, the presence of MET amplification is a predictor of high sensitivity to anti-MET compounds, and several agents have entered in clinical trials for patients having advanced disease, with promising results. The aim of the present review is to summarize available data on the role of MET in NSCLC and to describe therapeutic strategies under investigation.Keywords: mesenchymal-epidermal transition, hepatocyte growth factor, epidermal growth factor receptor, non-small cell lung cancerLandi LMinuti GD&#39;Incecco ASalvini JCappuzzo FDove Medical PressarticleNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENLung Cancer: Targets and Therapy, Vol 2013, Iss default, Pp 15-25 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282
spellingShingle	Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Landi L Minuti G D&#39;Incecco A Salvini J Cappuzzo F MET overexpression and gene amplification in NSCLC: a clinical perspective
description	Lorenza Landi, Gabriele Minuti, Armida D'Incecco, Jessica Salvini, Federico CappuzzoMedical Oncology Department, Istituto Toscano Tumori, Ospedale Civile, Livorno, ItalyAbstract: The transmembrane tyrosine kinase mesenchymal-epidermal transition (MET) receptor and its ligand, hepatocyte growth factor, also known as scatter factor, have recently been identified as novel promising targets in several human malignancies, including non-small cell lung cancer (NSCLC). Amplification, mutation, or overexpression of the MET gene can result in aberrant activation of the MET axis, leading to migration, invasion, proliferation, metastasis, and neoangiogenesis of cancer cells, suggesting that interfering with the MET/hepatocyte growth factor pathway could represent a potential antitumor strategy. While the role of MET mutations in NSCLC is not as yet fully understood, retrospective studies have shown that an increased MET gene copy number is a negative prognostic factor. In NSCLC, amplification of the MET gene is a relatively rare event, occurring in approximately 4% of patients not previously exposed to systemic therapies and in up to 20% of patients with acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors. In preclinical models, the presence of MET amplification is a predictor of high sensitivity to anti-MET compounds, and several agents have entered in clinical trials for patients having advanced disease, with promising results. The aim of the present review is to summarize available data on the role of MET in NSCLC and to describe therapeutic strategies under investigation.Keywords: mesenchymal-epidermal transition, hepatocyte growth factor, epidermal growth factor receptor, non-small cell lung cancer
format	article
author	Landi L Minuti G D&#39;Incecco A Salvini J Cappuzzo F
author_facet	Landi L Minuti G D&#39;Incecco A Salvini J Cappuzzo F
author_sort	Landi L
title	MET overexpression and gene amplification in NSCLC: a clinical perspective
title_short	MET overexpression and gene amplification in NSCLC: a clinical perspective
title_full	MET overexpression and gene amplification in NSCLC: a clinical perspective
title_fullStr	MET overexpression and gene amplification in NSCLC: a clinical perspective
title_full_unstemmed	MET overexpression and gene amplification in NSCLC: a clinical perspective
title_sort	met overexpression and gene amplification in nsclc: a clinical perspective
publisher	Dove Medical Press
publishDate	2013
url	https://doaj.org/article/22c9f43c6aca43b68b29d128428afaee
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MET overexpression and gene amplification in NSCLC: a clinical perspective

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