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• W2585501848 abstract "Proc Amer Assoc Cancer Res, Volume 45, 20044531 Introduction and Objective: Gefitinib (‘Iressa’, ZD1839) is an orally active EGFR-TKI (epidermal growth factor receptor tyrosine kinase inhibitor) that is currently being studied in Phase II clinical trials in bladder cancer patients. We investigated the antiproliferative activity of gefitinib on bladder cancer cells displaying various levels of EGFR expression (235J-BV, UC-3, UC-13, and KU-7) and its effect in increasing the cells’ sensitivity to docetaxel. Method: The antiproliferative effects of gefitinib and docetaxel were measured at 48 h in the presence of EGF or serum using the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay, which measures the metabolic activity of living cells. EGFR phosphorylation was measured using phospho-specific antibodies against various EGFR phosphorylation sites. The effects of gefitinib on actin rearrangement, cell motility, and invasion were demonstrated using immunofluorescence staining followed by confocal microscopy and in vitro Boyden chamber invasion assays. Apoptosis and cell-cycle analysis were evaluated 24 and 48 h after treatment using propidium iodide and flow cytometry. Results: EGFR phosphorylation was totally blocked by 1 mM in KU-7, UC-3, and UC-13 cells. The IC50 of gefitinib on cell proliferation was observed at 10 nM in 235J-BV cells, and these cells also displayed the highest level of EGFR expression. In 235J-BV cells, gefitinib treatment induced a dose-dependent G0/G1 cellular arrest with decreased S-phase and no sub-G0/G1 population (apoptosis) after 48 h. Docetaxel (10 nM) alone induced a total G2/M arrest with 28% of cells in sub-G0/G1 phase (apoptotic). The combination of gefitinib and docetaxel had no additive effect on apoptosis compared with docetaxel alone and cells were arrested in both G0/G1 and G2/M phases. Cells with very low EGFR expression levels, such as UC-3, showed resistance to the antiproliferative effect of gefitinib and no apoptotic effect for concentrations up to 5 mM. However, the combination of gefitinib (0.5 mM) and docetaxel (10 nM) resulted in 48% apoptosis in UC-3 cells and G2/M cell arrest compared with only 24% apoptosis with docetaxel alone. Interestingly, gefitinib concentrations up to 0.5 mM induced a significant inhibitory effect on cellular invasion potential in all cells tested, including UC-3 cells. Conclusion: Gefitinib can inhibit invasion and cell proliferation with G0/G1 arrest and can affect cell survival depending on EGFR expression and activation levels in bladder cancer cells. Gefitinib treatment followed by docetaxel-containing regimens may represent a way to potentiate the chemotherapeutic effect of docetaxel-containing combinations, especially in cells displaying trace amounts of EGFR. ‘Iressa’ is a trademark of the AstraZeneca group of companies." @default.
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• W2585501848 date "2004-04-01" @default.
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• W2585501848 title "Antitumor effect and potentiation of docetaxel activity in human bladder cancer cells treated with gefitinib (‘Iressa’, ZD1839)" @default.
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