Scientific publications

cMET in NSCLC: Can We Cut off the Head of the Hydra? From the Pathway to the Resistance

Van Der Steen N(1), Pauwels P(2,3), Gil-Bazo I(4), Castañon E(5,6), Raez L(7), Cappuzzo F(8), Rolfo C(9,10).
(1) Center for Oncological Research Antwerp, University of Antwerp, Universiteitsplein 1, Wilrijk 2610, Belgium.
(2) Center for Oncological Research Antwerp, University of Antwerp, Universiteitsplein 1, Wilrijk 2610, Belgium.
(3) Molecular Pathology Unit, Pathology Department, Antwerp University Hospital, Wilrijkstraat 10, Edegem 2650, Belgium.
(4) Department of Oncology, Clínica Universidad de Navarra, Pamplona 31008, Spain.
(5) Department of Oncology, Clínica Universidad de Navarra, Pamplona 31008, Spain. 
(6) Phase I-Early Clinical Trials Unit, Oncology Department, Antwerp University Hospital, Wilrijkstraat 10, Edegem 2650, Belgium.
(7) Thoracic Oncology Program, Memorial Cancer Institute, Memorial Health Care System, Pembroke Pines, FL 33024, USA.
(8) Medical Oncology Department, Istituto Toscano Tumori, Ospedale Civile, Livorno, Italy viale Alfieri 36, Livorno 57100, Italy.
(9) Center for Oncological Research Antwerp, University of Antwerp, Universiteitsplein 1, Wilrijk 2610, Belgium.
(10) Phase I-Early Clinical Trials Unit, Oncology Department, Antwerp University Hospital, Wilrijkstraat 10, Edegem 2650, Belgium.

Magazine: Cancers

Date: Mar 25, 2015

Medical Oncology

Abstract

In the last decade, the tyrosine kinase receptor cMET, together with its ligand hepatocyte growth factor (HGF), has become a target in non-small cell lung cancer (NSCLC).

Signalization via cMET stimulates several oncological processes amongst which are cell motility, invasion and metastasis. It also confers resistance against several currently used targeted therapies, e.g., epidermal growth factor receptor (EGFR) inhibitors.

In this review, we will discuss the basic structure of cMET and the most important signaling pathways. We will also look into aberrations in the signaling and the effects thereof in cancer growth, with the focus on NSCLC. Finally, we will discuss the role of cMET as resistance mechanism.

CITATION  Cancers (Basel). 2015 Mar 25;7(2):556-73. doi: 10.3390/cancers7020556.

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