Abstract
Background: Epidermal growth factor receptor (EGFR) is a transmembrane protein. That is a receptor for members of epidermal growth factor family (EGF family) of extracellular protein ligand. The EGFR is a member of the erb family of receptor, a subfamily of four closely related receptor tyrosine kinase - EGFR (erb B-1), Her2/neu(erb B-2), Her3 (erb B-3) and Her4 (erb B-4). Over expression of EGFR is commonly noted in breast, bladder and lung carcinoma. Amplified EGFR gene has also been observed in a number of high grade brain tumour, glioblastoma multiforme (Grade IV) in particular.
Material and Methods: A retrospective study of four years (2012 October to 2016 September) and one and half years prospective (2016 October to 2018 April) study was carried out in IMS & SUM Hospital in collaboration with Neurosurgery department and the follow up was done for a period of 1 year. All CNS tumours were subjected to squash and frozen section followed by histo-pathologic biopsy. The inclusion criteria were all the glioma cases with the patients’ age ranging from 5 to 85 years. This was further subjected to IHC study of EGFR.
Results and Observation: It was found that EGFR expression was negative in low grade glioma like pilocytic astrocytoma, diffuse astrocytoma, oligodendroglioma and ependymomas, whereas EGFR is was positive in high grade gliomas (grade III & IV) like anaplastic astrocytoma and glioblastoma. Amongst the GBM, 80% were primary which showed 100% EGFR positivity where as only 20% of secondary GBM showed EGFR positivity and amongst the variants of GBM, gliosarcoma showed EGFR negativity in contrast to other subtypes.
Conclusion: EGFR can be used as a prognostic marker in gliomas, especially to distinguish between low grade type and high grade type and primary with secondary GBM. But therapeutic success of tyrosine kinase inhibitor that target EGFR has produced encouraging results.
Study type and design: Hospital based cross sectional study and an observational study.
Keywords: EGFR, Glioma, CNS, GBM, Tyrosine kinase inhibitors.
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Corresponding Author
Debahuti Mohapatra
Prof. & Head, Dept. of Pathology, IMS & SUM Hospital, BBSR- 751003, Odisha, India
Email: This email address is being protected from spambots. You need JavaScript enabled to view it., Cell – 09439831760
DOI: https://dx.doi.org/10.18535/jmscr/v7i2.127
