Abstract

<div>Abstract<p><b>Background:</b> The epidermal growth factor receptor (EGFR) regulates important cellular processes and is frequently implicated in human tumors. Three <i>EGFR</i> polymorphisms have been described as having a transcriptional regulatory function: two single-nucleotide polymorphisms in the essential promoter region, −216G/T and −191C/A, and a polymorphic (CA)<sub>n</sub> microsatellite sequence in intron 1. We aimed to elucidate the roles of these <i>EGFR</i> polymorphisms in glioma susceptibility and prognosis.</p><p><b>Methods:</b> We conducted a case–control study with 196 patients with glioma and 168 cancer-free controls. Unconditional multivariate logistic regression models were used to calculate ORs and 95% confidence intervals. A Cox regression model was used to evaluate associations with patient survival. False-positive report probabilities were also assessed.</p><p><b>Results:</b> None of the <i>EGFR</i> −216G/T variants was significantly associated with glioma risk. The −191C/A genotype was associated with higher risk for glioma when the (CA)<sub>n</sub> alleles were classified as short for ≤16 or ≤17 repeats. Independently of the (CA)<sub>n</sub> repeat cutoff point used, shorter (CA)<sub>n</sub> repeat variants were significantly associated with increased risk for glioma, particularly glioblastoma and oligodendroglioma. In all tested models with different (CA)<sub>n</sub> cutoff points, only −191C/A genotype was consistently associated with improved survival of patients with glioblastoma.</p><p><b>Conclusions:</b> Our findings implicate <i>EGFR</i> −191C/A and the (CA)<sub>n</sub> repeat polymorphisms as risk factors for gliomas, and suggest −191C/A as a prognostic marker in glioblastoma.</p><p><b>Impact:</b> Our data support a role of these <i>EGFR</i> polymorphisms in determining glioma susceptibility, with potential relevance for molecularly based stratification of patients with glioblastoma for individualized therapies. <i>Cancer Epidemiol Biomarkers Prev; 20(12); 2610–7. ©2011 AACR</i>.</p></div>

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