Treatment of cultured glioma cells with EGFR-TKI gefitinib (‘Iressa’, ZD1839) increases the uptake of astatinated EGF despite absence of gefitinib-mediated growth inhibition
2003 (English)In: European Journal of Nuclear Medicine, ISSN 0340-6997, Vol. 30, no 5, 727-9 p.Article in journal (Refereed) Published
The EGFR-TKI (epidermal growth factor receptor tyrosine kinase inhibitor) gefitinib ("Iressa", ZD1839), a reversible growth inhibitor of EGFR-expressing 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 ((211)At-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 (211)At-EGF in U343 cells was markedly increased (up to 3.5 times) in cells pre-treated with gefitinib (1 microM). 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.
Place, publisher, year, edition, pages
2003. Vol. 30, no 5, 727-9 p.
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:uu:diva-64295DOI: 10.1007/s00259-003-1129-xPubMedID: 12740721OAI: oai:DiVA.org:uu-64295DiVA: diva2:92206