Asia Oceania Journal of Nuclear Medicine and Biology

Asia Oceania Journal of Nuclear Medicine and Biology

Assessment of epidermal growth factor receptor status in glioblastomas

Document Type : Original Article

Authors
Hui-Jun Zhu 1
Harumi Sakahara 1
Mikako Ogawa 2
Yasuhiro Magata 2
Yoshiro Ohmomo 3
Masahiko Hirata 3
Hiroki Namba 4
1 Department of Radiology Hamamatsu University of School of Medicine, Japan
2 Medical Photonics Research Center, Hamamatsu University School of Medicine, Japan
3 Osaka University of Pharmaceutical Sciences, Japan
4 Department of Radiology, Hamamatsu University School of Medicine, Japan
10.7508/aojnmb.2013.02.007
Abstract
Objective(s): Our previous study showed that a newly designed tracer radioiodinated 6-(3-morpholinopropoxy)-7-ethoxy-4-(3'-iodophenoxy)quinazoline ([125I]PYK) is promising for the evaluation of the epidermal growth factor receptor (EGFR) status and prediction of gefitinib treatment of non-small cell lung cancer. EGFR is over-expressed and mutated also in glioblastoma. In the present study, the expressions and mutation of EGFR were tested with [125I] PYK in glioblastoma in vitro and in vivo to determine whether this could be used to predict the sensitivity of glioblastoma to gefitinib treatment.
Methods: Glioblastoma cell lines with different expression of EGFR were tested. Growth inhibition of cell lines by gefitinib was assessed by the 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) colorimetric assay. Uptake levels of [125I]PYK were evaluated in cell lines in vitro. Tumor targeting of [125I]PYK was examined by a biodistribution study and imaging by single photon emission computed tomography (SPECT).
Results: High concentrations of gefitinib were needed to suppress EGFR-mediated proliferation. The uptake of [125I] PYK in cell lines in vitro was low, and showed no correlation with EGFR expression or mutation status. Biodistribution study and SPECT imaging with [125I]PYK for xenografts showed no [125I]PYK uptake.
Conclusion: The results showed prediction of gefitinib effectiveness was difficult in glioblastoma by [125I]PYK, which might be due to the complicated expression of EGFR status in glioblastoma. Thus, new tracers for sites downstream of the mutant EGFR should be investigated in further studies.
Keywords
[125I]PYK
Gefitinib
EGFR
Glioblastoma
Subjects
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Asia Oceania Journal of Nuclear Medicine and Biology
Volume 1, Issue 2 - Serial Number 2
October 2013
Pages 47-52