alexa Signaling Pathways Supporting Tumor Invasion in Head and Neck Squamous Cell Carcinoma | OMICS International| Abstract
ISSN: 2161-0681

Journal of Clinical & Experimental Pathology
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  • Review Article   
  • J Clin Exp Pathol 2014, Vol 5(3): 227
  • DOI: 10.4172/2161-0681.1000227

Signaling Pathways Supporting Tumor Invasion in Head and Neck Squamous Cell Carcinoma

Michal Kidacki, Heather L Lehman, Joshua I Warrick and Douglas B Stairs*
Department of Pathology, The Pennsylvania State University College of Medicine, 500 University Drive, Hershey, Pennsylvania, USA
*Corresponding Author : Douglas B Stairs, Assistant Professor of Pathology, Pharmacology and Biochemistry & Molecular
Biology Medical Director, Morphologic and Molecular Core Research Laboratory, 500 University Drive, Hershey, Pennsylvania 17033, USA, Tel: 7175316725, Email: [email protected]

Received Date: Mar 25, 2015 / Accepted Date: May 18, 2015 / Published Date: May 21, 2015

Abstract

Head and neck squamous cell carcinoma (HNSCC) is a highly invasive cancer. A number of signaling pathways like PI3K, Rho and TGFβ/SMAD drive the invasive nature of HNSCC. The PI3K pathway is the most altered pathway in HNSCC. Both upstream and downstream members of this pathway have been found to be mutated or overexpressed leading to an increase in cell invasion. The Rho pathway is also commonly activated; however, only overexpression or downregulation of Rho’s upstream regulators are found in HNSCC. Finally, TGFβ/SMAD pathway activation leads to epithelial mesenchymal transition in HNSCC and subsequently invasion, though loss of TGFβ/ SMAD signaling has also been shown to increase cell invasion.

Keywords: Invasion; HNSCC; PI3K; EGFR; Rho; SMAD; TGFβ

Citation: Kidacki M, Lehman HL, Warrick JI, Stairs DB (2015) Signaling Pathways Supporting Tumor Invasion in Head and Neck Squamous Cell Carcinoma. J Clin Exp Pathol 5:227. Doi: 10.4172/2161-0681.1000227

Copyright: ©2015 Kidacki M, 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.

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