For example, lung cancer cell-lines show different sensitivities to doxorubicin in the form of GSH depletion, with A549 and GLC 4 210(S) cells experiencing approximately 50% and 64% GSH depletion after a 12 hour exposure to 70 nM and 5 nM (per million cells) respectively 37
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Here we report that these two oncogenic pathways may not act in concert, but act apparently partially antagonistic at least in human GIC models, potentially accounting for disappointing results with inhibition of either pathway in the clinic 29,30,31 , but also providing new concepts on how to modulate these pathways more efficiently to improve the outcome of glioblastoma
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