NDLI: Analysis of EGFR Gene Amplification, Protein Over-expression and Tyrosine Kinase Domain Mutation in Recurrent Glioblastoma

Content Provider	Springer Nature Link
Author	Toth, Judit Egervari, Kristof Klekner, Almos Bognar, Laszlo Szanto, Jas Nemes, Zoltan Szollosi, Zoltan
Copyright Year	2008
Abstract	Gefitinib and erlotinib are both selective EGFR tyrosine kinase inhibitors (EGFR-TKIs) that have produced responses in a small subgroup of lung cancer patients. The strongest evidence for a role of EGFR in the biology of glioblastoma stems from clinical trials in which 15–20% of recurrent glioblastoma patients experienced significant tumour regression in response to these small-molecule EGFR kinase inhibitors. We examined the protein-kinase domain of the EGFR gene, EGFR protein expression and EGFR gene amplification in 20 cases of recurrent GBMs. EGFR protein over-expression was found in 65% of cases. EGFR protein over-expression was associated with EGFR gene amplification in 35% of cases, and with high polysomy in 15% of cases. No mutations were found in the TK domain of the EGFR gene. Our results confirm that mutations in the kinase domain are absent in recurrent GBM, and this might be a preponderant factor in the lack of major clinical responses of TKIs in GBM, recent studies have suggested that responsiveness to EGFR kinase inhibitors was strongly associated with coexpression of EGFRvIII and PTEN. Further prospective validation of EGFRvIII and PTEN as predictors of the clinical response to EGFR kinase inhibitors in recurrent GBM is strongly anticipated.
Starting Page	225
Ending Page	229
Page Count	5
File Format	PDF
ISSN	12194956
Journal	Pathology & Oncology Research
Volume Number	15
Issue Number	2
e-ISSN	15322807
Language	English
Publisher	Springer Netherlands
Publisher Date	2008-08-28
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	Glioblastoma multiforme EGFR Kinase inhibitor treatment Biomedicine general Immunology Pathology Oncology Cancer Research
Content Type	Text
Resource Type	Article
Subject	Cancer Research Pathology and Forensic Medicine Oncology

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