Treatment of cultured glioma cells with the EGFR-TKI gefitinib ("Iressa", ZD1839) increases the uptake of astatinated EGF despite the absence of gefitinib-mediated growth inhibition

Åsa Liljegren Sundberg, Ylva Almqvist, Vladimir Tolmachev, Jörgen Carlsson

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)

Abstract

The EGFR-TKI (epidermal growth factor receptor tyrosine kinase inhibitor) gefitinib ("Iressa", ZD1839), a reversible growth inhibitor of EGFRexpressing tumour cells, has been shown to enhance the antitumour effect of ionising radiation, and also to increase the uptake of radioiodinated EGF. Thus, combination of gefitinib treatment and radionuclide targeting is an interesting option for therapy of brain tumours that are difficult to treat with conventional methods. The aim of this study was to evaluate how pre-treatment with gefitinib affects binding of astatinated EGF (211At-EGF) to cultured glioma U343 cells, which express high levels of EGFR. The growth of U343 cells in the presence of gefitinib was investigated, and it was found that gefitinib does not significantly inhibit the growth of these cells. Nevertheless, the uptake of 211At-EGF in U343 cells was markedly increased (up to 3.5 times) in cells pre-treated with gefitinib (1 μM). This indicates that a combination of gefitinib treatment and radionuclide targeting to EGFR might be a useful therapeutic modality, even for patients who do not respond to treatment with gefitinib alone.

Original languageEnglish
Pages (from-to)727-729
Number of pages3
JournalEuropean Journal of Nuclear Medicine and Molecular Imaging
Volume30
Issue number5
DOIs
Publication statusPublished - 1 May 2003
Externally publishedYes

Keywords

  • EGFR
  • Gefitinib
  • Glioma

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging

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