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PTEN-inactivation in glioblastoma (GBM) triggers the hyperactivation of protein kinases, including mTOR and its downstream target, the ribosomal protein S6 kinase 1 (S6K1). Previous studies have demonstrated the potential efficacy of mTOR inhibitors for GBM therapy. We explored S6K1 inhibitors for potential cytotoxic effects in PTEN-deficient GBM cells. All S6K1 inhibitors were effective in reducing the phosphorylation of S6K1 substrates. However, analysis of the phosphorylation of thedoi:10.1093/neuonc/nov204.66 fatcat:55v2jsbd45gbvpmfbtta7tu4oq