EGFR as a clinical marker in glioblastomas and other gliomas

• Published in: The International Journal of Biological Markers Vol. 33; no. 1; pp. 22 - 32
• Main Authors: Saadeh, Fadi S., Mahfouz, Rami, Assi, Hazem I.
• Format: Book Review Journal Article
• Language: English
• Published: London, England SAGE Publications 01.01.2018; Sage Publications Ltd
• Subjects: Brain tumors; Copy number; Epidermal growth factor; Epidermal growth factor receptors; Glial cells; Glioma; Kinases; Medical prognosis; Protein-tyrosine kinase; Single-nucleotide polymorphism; Prognosis; Glioma; Tyrosine kinase inhibitor; Epidermal growth factor receptor; Glioblastoma
• ISSN: 1724-6008; 0393-6155; 1724-6008
• DOI: 10.5301/ijbm.5000301

Epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein and a member of the tyrosine kinase superfamily receptor. Gliomas are tumors originating from glial cells, which show a range of aggressiveness depending on grade and stage. Many EGFR gene alterations have been identified in gliomas, especially glioblastomas, including amplifications, deletions and single nucleotide polymorphisms (SNPs). Glioblastomas are discussed as a separate entity due to their high correlation with EGFR mutants and the reported association of the latter with survival and response to treatment in this glioma subgroup. This review is a comprehensive report of EGFR gene alterations and their relations with several clinical factors in glioblastomas and other gliomas. It covers all EGFR gene alterations including point mutations, SNPs, methylations, copy number variations and amplifications, assessed with regard to different clinical variables, including response to therapy and survival. This review also discusses the current prognostic status of EGFR in glioblastomas and other gliomas, and highlights gaps in previous studies. This serves as an update for the medical community about the role of EGFR gene alterations in gliomas and specifically glioblastomas, as a means for targeted treatment and prognosis.