Assessment of epidermal growth factor receptor status in glioblastomas

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. materials and 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