Evaluation of Nestin and EGFR in Patients with Glioblastoma Multiforme in a Public Hospital in Iran

Matini, Amir Hassan; Mofidi Naeini, Mohadeseh; Haddad Kashani, Hamed; Vakili, Zarichehr

doi:10.31557/APJCP.2020.21.10.2889

Evaluation of Nestin and EGFR in Patients with Glioblastoma Multiforme in a Public Hospital in Iran

Document Type : Research Articles

Authors

¹ Department of Pathology, Kashan University of Medical Sciences, Kashan, Iran.

² Anatomical Sciences Research Center, Basic Sciences Research Institute, Kashan University of Medical Sciences, Kashan, Iran.

10.31557/APJCP.2020.21.10.2889

Abstract

Introduction: Glioblastoma multiforme (GBM) is a grade IV glioma and accounts for 15% of all primary brain tumors. This GBM has a median survival range of less than 2 years after diagnosis and it is highly vascularized by neoformed vessels. Neoangiogenesis is a crucial factor in the malignant tumoral behavior and prognosis of patients and Nestin protein belongs to class VI which is expressed in endothelial cells of neoformed vessels in GBM. Our study shows the correlation between EGFR mutation and Nestin expression in endothelial of neoformed vessels in GBM. Methods: We analyzed 40 GBM samples by immunohistochemistry staining. The immunohistochemical expression of EGFR in tumoral cells and Nestin in endothelial cells in paraffin sections were analyzed. EGFR scoring was the based on staining intensity. Score 0 shows No staining, Score1, mild to moderate staining and score2 sever staining. Microvascular density (MVD) was evaluated with Nestin-immunoreactive. Results: The mean of MVD was 14.6 ±8.25. Nestin-MVD was significantly higher in GBM with sever vascular prolifration (p-value=0.01). EGFR was expressed in 92.5% of samples. The EGFR scoring for tumoral tissue was 7.5%(score:0), 22.5% (score:1) and 70% (score:2). There was a significant relationship between EGFR expression and MVD (p-value=0.017). Conclusion: We suggest that some important mutations as like as EGFR in GBM is responsible for inducing angiogenesis and vascular proliferation. Nestin overexpression as a novel marker might reflect the extent of neoangiogenesis, thus target therapy against EGFR pathway and anti angiogenic may be useful for GBM treatment.

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