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ISSN: 2167-7700

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Research Article

c-Met: A Potential Target for Current Non-Small-Cell Lung Cancer Therapeutics

Amanda Stone1+, Supriya Rajanna1, Ichwaku Rastogi1, Joe Cruz1, Kymberly Harrington1, Kory Blank2, Mark Frakes2 and Neelu Puri1*+

1University of Illinois at Rockford, Department of Biomedical Sciences, USA

2University of Illinois at Rockford, College of Medicine, USA

+Both authors have contributed equally to this work

*Corresponding Author:
Neelu Puri, Ph.D
Assistant Professor
University of Illinois College of Medicine at Rockford
Department of Biomedical Sciences
1601 Parkview Avenue, Rockford, Illinois 61107, USA
Tel: 815-395-5678
Fax: 815-395-5666
E-mail: [email protected]

Received date: July 18, 2014; Accepted date: July 24, 2014; Published date: July 28, 2014

Citation: Stone A, Rajanna S, Rastogi I, Cruz J, Harrington K (2014) c-Met: A Potential Target for Current Non-Small-Cell Lung Cancer Therapeutics. Chemotherapy 3:136. doi:10.4172/2167-7700.1000136

Copyright: © 2014 Stone A et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. In early stages of NSCLC tumor development (stage I/II), surgical resection is often performed; however, when the cancer becomes metastatic, chemotherapy is most commonly implemented. Due to the fact that traditional chemotherapies result in adverse and cytotoxic effects on healthy cells in addition to NSCLC cells, targeted therapeutics have been extensively developed over recent years to combat the disease. These targeted therapies include small molecule inhibitors and monoclonal antibodies (MAbs), some of which are used as first-line treatments for NSCLC patients. Several inhibitors against the mesenchymal-epithelial transition factor (c-Met), and its ligand hepatocyte growth factor (HGF), have shown promising results in NSCLC clinical trials. For example, crizotinib, a multi-kinase inhibitor has been approved by the FDA for the treatment of ALK positive NSCLC. c-Met is known to be overexpressed, mutated and gene amplified, specifically in NSCLC, and has also been implicated in the development of resistance against other small-molecule inhibitors (e.g. EGFR). Thus, this review will discuss the current developments and usages of c-Met inhibitors in NSCLC, and their potential for future therapeutic advancement.

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