Abstract

Abstract Recently, there is growing evidence to support that oral cavity and oropharyngeal squamous cell carcinoma are two distinct diseases with different etiology. The aim of this study was to evaluate the expression of EGFR, PI3K/Akt/mTOR pathway, and PTEN in oral cavity and oropharyngeal cancers, and to investigate their clinical significance as prognostic markers. One hundred twenty-one patients who underwent curative surgery for oral cavity or oropharyngeal squamous cell carcinoma in Seoul St. Mary's Hospital between January 1995 and September 2009 were evaluated. The level of protein expression of EGFR, PIK3CA, pAkt, mTOR, and PTEN was assessed by immunohistochemistry. In situ hybridization was used for assessment of human papillomaviruses (HPV). Nineteen of 61 patients with oropharyngeal cancer showed HPV-positive tumors, and 2 of 60 patients with oral cavity cancer showed HPV-positive tumors. EGFR and pAkt expression were significantly higher in oray cavity cancer than in oropharyngeal cancer. Loss of PTEN was significantly higher in oral cavity cancer than in oropharyngeal cancer. There were no significant differences in PIK3CA, mTOR, and p53 expressions. HPV-negative tumors overexpressed more EGFR and pAkt than HPV-positive tumors. Loss of PTEN expression was more frequent in HPV-negative tumors than in HPV-positive tumors. In multivariate cox regression analysis, pAkt expression showed a significant impact on relapse-free survival. There was a significantly negative correlation between PTEN and pAkt expression, and positive correlation between pAkt and mTOR expression. We concluded that there were differences in expression of EGFR, pAkt, and PTEN between oropharyngeal and oral cavity cancer. It was attributed to etiologic role of human papillomaviruses in oropharyngeal cancer. The expression of pAkt may be a prognostic marker for relapse-free survival in oropharyngeal cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2011 Nov 12-16; San Francisco, CA. Philadelphia (PA): AACR; Mol Cancer Ther 2011;10(11 Suppl):Abstract nr B21.

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