Abstract:
Gliomas are the common brain tumor in adults, accounting for about 70% of primary neoplasms
of the Central Nervous System (CNS). Glioblastoma (GBM) is the most popular glioma, accounting
for approximately 70% of astrocytomas and 15% of all intracranial neoplasms. 90% of GBMs are
classified as primary, affect mainly the older (mean age 62 years), have rapid progression (less than 3
months) and no evidence of previous clinical or histopathological precursor lesions [1]. Secondary
GBMs are common in young individuals (average age 45 years) and progress slowly from a lower
grade of diffuse astrocytoma, the two forms of GBM have worse prognosis. Histological analysis
can only define the type of an astrocytic neoplasm and diagnostic difficulties may happen due to
the diversity of the tumor, morphological similarity with other gliomas or partial sampling of the
lesion. As a result, in recent decades, several studies have used molecular techniques aiming to
define biomarkers with diagnostic and/or prognostic relevance, which allowed the identification
of such markers and significantly increased the knowledge of the pathogenesis of gliomas, and
identification of potential targets for new therapeutic approaches [1-3]. Epidermal Growth Factor
Receptor (EGFR) is one of ErbB family receptors with tyrosine kinase activity [4,5]. EGFR is
frequently over expressed or hyper-activated in human malignancies. Increased activation of EGFR
can be both ligand-dependent and ligand-independent [6-8]. Mechanisms of increased activation
include: Aberrant enhancement of ligand production; constitutive receptor activation by multiple
exon deletion or missense mutations [9]; crosstalk with other receptors; increased receptor protein
level through gene amplification; and malfunction in receptor degradation. EGFR over expression
