作者: Detlef Bartkowiak , Peter R. Hipp , Marc S. Mendonca , Erwin M. Röttinger
DOI: 10.1007/S00066-007-1680-7
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摘要: Purpose: To study the radiation response-modifying effect of imatinib (Gleevec®) in a squamous cell carcinoma line, PECA. Material and Methods: Cytotoxicity was determined by colony forming multiplying capacity. Drug stability shown HPLC. Multidrug resistance phenotype studied rhodamine-123 efflux. Cell-cycle responses were measured flow cytometry. Homologous recombination repair Rad51 immunohistochemistry. Results: Inactivating 50% PECA cells required approximately 7 µM imatinib. The drug did not decay nor it degraded during test periods. efflux occurred only to minor extent. Multiplying capacity but survival fractions revealed radioprotective There cell-cycle alterations presence rate Rad51-positive foci significantly increased. Conclusion: apparently lack highly specific target for In surviving at high concentrations, may exert on inducing DNA repair. Under prolonged exposure, drug-resistant show an accelerated recovery from acute or delayed damage.