Abstract 448: Elevated co-expression of HIF-1α and GLUT-1 is associated with poor prognosis for oral squamous cell carcinoma patients

2010 
Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC HIF1α is the key transcriptional regulator of the response to hypoxia in tumors. GLUT-1 is a HIF1α-dependent target gene that is upregulated under hypoxic conditions and enables glucose transport into tumor cells. We sought to identify if co-expression of both of these hypoxia-related proteins, as detected by immunohistochemistry, had prognostic relevance in oral squamous cell carcinomas [OSCC]. Eighty-two OSCC tumor samples were analyzed for their expression levels of both HIF1α and GLUT-1 by immunohistochemistry. Protein expression was assessed using an immunoreactive score system (IRS) and the correlation between gene expression and both clinical and pathohistological parameters were examined. Overexpression of either GLUT-1 or HIF1α was associated with poor overall survival in OSCC patients. Multivariate Cox's proportional-hazards regression analysis (adjusted for tumor size and tumor grade) revealed that moderate expression of GLUT-1 or HIF1α was significantly associated with overall survival (RR=5.07, p=0.002 and RR=4.5, p=0.017, respectively) as compared to the groups with low levels of expression of GLUT-1 or HIF1α. Co-expression of both HIF1α and GLUT-1 were additively and significantly associated with adverse prognoses in patients with OSCC. Patients whose tumors had high levels of expression of both HIF1α and GLUT-1 were found to have a 10.2-fold increased risk of tumor-related death (p=0.001) in the multivariate Cox's proportional-hazards regression analysis. Co-expression of high levels of HIF1α and GLUT-1 is significantly correlated with prognosis in OSCC patients, suggesting that the co-expression of these proteins can be used as both an early diagnostic and independent prognostic marker. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 448.
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