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Journal of Environmental Pathology, Toxicology and Oncology
Fator do impacto: 1.241 FI de cinco anos: 1.349 SJR: 0.356 SNIP: 0.613 CiteScore™: 1.61

ISSN Imprimir: 0731-8898
ISSN On-line: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvPathToxOncol.v24.i3.20
pages 149-162

Role of c-MET in Upper Aerodigestive Malignancies — From Biology to Novel Therapies

Sascha Dietrich
Section of Hematology/Oncology, Department of Medicine, The University of Chicago, Pritzker School of Medicine, and The University of Chicago, Cancer Research Center, Chicago, Illinois, USA
Radha Uppalapati
Section of Hematology/Oncology, Department of Medicine, The University of Chicago, Pritzker School of Medicine, and The University of Chicago, Cancer Research Center, Chicago, Illinois, USA
Tanguy Y. Seiwert
Section of Hematology/Oncology, Department of Medicine, The University of Chicago, Pritzker School of Medicine, and The University of Chicago, Cancer Research Center, Chicago, Illinois, USA
Patrick C. Ma
Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute; Brigham and Women’s Hospital; Harvard Medical School; Tufts-New England Medical Center, Boston, Massachusetts;University of Chicago, Pritzker School of Medicine, Chicago, Illinois, USA

RESUMO

Overactivation and defective downregulation of receptor tyrosine kinase (RTK) pathways have been implicated in human carcinogenesis. RTKs represent an important class of anticancer novel therapeutic target. Some RTKs are known to be protooncogenes that can mediate signal transduction, alteration of reactive oxygen species (ROS), cellular proliferation, cell motility and migration, apoptosis, and survival. c-MET is a unique RTK that regulates a wide variety of cellular functions. c-MET has been shown to be overexpressed or mutated in a variety of human malignancies. Stimulation of c-MET via its natural ligand hepatocyte growth factor/ scatter factor (HGF/SF) leads to a plethora of biological and biochemical effects in the cell. Activation of c-MET signaling can lead to cell motility and scattering, angiogenesis, proliferation, branching morphogenesis, invasion, and eventual metastasis. This review summarizes the structure and functions of c-MET, with particular emphasis on its role in upper aerodigestive malignancies. The unique biological functions altered by c-MET and its mutations are discussed as well. Fınally, c-MET, when mutated or overexpressed in malignant cells, serves as an important therapeutic target, and the most recent data with respect to its inhibition are also summarized in this review.


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