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Glioblastoma multiforme (GBM) is the most common primary brain tumor among adults. Rapid tumor progression and diffuse invasion of brain tissue restrict the therapeutic options and result in poor prognosis despite advances in the understanding of this tumor’s molecular biology and pathophysiology [1-4]. Current standard therapy consists of a combination of tumor resection, irradiation and temozolomide. Advances in the field of molecular biology have led to the development of targeted therapy, and the epidermal growth factor receptor (EGFR) has been introduced as one potential therapeutic target [5]. Although pre-clinical studies have shown promising effects, clinical applications yielded no significant benefit in comparison with standard therapy. This fact encouraged extensive investigations studying the molecular mechanisms underlying GBM resistance to EGFR-targeted therapy. Epithelial to mesenchymal transition (EMT) is considered an important factor contributing to resistance towards this therapy by diminishing the molecular target [1-6].

Epithelial to Mesenchymal Transition and Progression of Glioblastoma