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EGFR as a clinical marker in glioblastomas and other gliomas

Abstract

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.

Post author correction

Article Type: REVIEW

DOI:10.5301/ijbm.5000301

Authors

Fadi S. Saadeh, Rami Mahfouz, Hazem I. Assi

Article History

Disclosures

Financial support: No grants or funding have been received for this study.
Conflict of interest: All authors declare they have no conflict of interest.

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Authors

Affiliations

  •  Faculty of Medicine, American University of Beirut, Beirut - Lebanon
  •  Department of Pathology and Laboratory Medicine, American University of Beirut Medical Center, Beirut - Lebanon
  •  Department of Internal Medicine, Naef K. Bassile Cancer Institute, American University of Beirut Medical Center, Beirut - Lebanon

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