Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

CiteULike is a free service for managing and discovering scholarly references - click here to get started.

Sign In to gain access to subscriptions and/or personal tools.
Journal of Dental Research
This Article
Right arrow Abstract Freely available
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow An erratum has been published
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Choi, S.
Right arrow Articles by Myers, J.N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Choi, S.
Right arrow Articles by Myers, J.N.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

Molecular Pathogenesis of Oral Squamous Cell Carcinoma: Implications for Therapy

S. Choi and J.N. Myers*

Department of Head and Neck Surgery, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 44, Houston, TX 77030-4009, USA


Figure 1
View larger version (16K):
[in this window]
[in a new window]

  		Figure 1. Genetic progression model of multistep oral carcinogenesis. Transformation of normal epithelium by multiple genetic alterations leads to dyplasia and invasive carcinoma. The acculumated genetic changes that occur in oral carcinogenesis include activation of the epidermal growth factor receptor (EGFR), alterations of tumor suppressors p53 and p16, and cyclin D1 overexpression. Adapted from Lippman et al.(2005).

 

Figure 2
View larger version (30K):
[in this window]
[in a new window]

  		Figure 2. Schematic representation of selected target agents in oral cancer. Signaling from growth factor receptor tyrosine kinases such as EGFR and VEGFR can be blocked by monoclonal antibodies or intracellular small-molecule tyrosine kinase inhibitors. In addition, other agents inhibiting Ras, Raf, mTOR, nuclear proteins, and intracytoplasmic proteins represent promising anti-cancer drugs. Adapted from Le Tourneau et al.(2007).

 

Journal of Dental Research, Vol. 87, No. 1, 14-32 (2008)
DOI: 10.1177/154405910808700104
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?