The epidermal growth factor receptor (EGFR) is a transmembrane tyrosine kinase receptor that plays a role in cell division, cell differentiation and migration.1
In cancer, EGFR is often mutated, amplified or overexpressed, resulting in abnormal receptor activation. Increased signaling by EGFR contributes to the proliferative nature of the malignant cells.3
Amplification, rearrangements, and mutations of the epidermal growth factor receptor (EGFR) gene are the most common genetic alterations in glioblastoma (GBM), with amplification occurring in approximately 50% of GBM tumors.3,5 EGFR amplification usually remains unchanged
at the time of tumor recurrence.7
EGFRvIII is the most frequently occurring EGFR mutation in GBM.3,6 The extracellular domain is truncated, resulting in ligand-independent constitutive activity.
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