Fig. 2
From: Activation of IGF1R/p110β/AKT/mTOR confers resistance to α-specific PI3K inhibition
BYL719 resistance correlates with increases in IGF1R, IRS (insulin receptor substrate), and p85 PI3K tyrosine phosphorylation. a Fold changes in tyrosine phosphorylation in resistant cells compared with parental cells without BYL719 treatment, expressed as the log2 resistant/parental ratio and displayed in rank order from low to high. Graphs were generated with TIBCO Spotfire software (TIBCO Software, Boston MA, USA). b Immunoblots of lysates from parental and resistant lines treated for 24 hours with 2 μM (T47D) or 5 μM (MCF7) BYL719 as indicated. c Bar graphs representing intensities of phosphopeptides bearing the indicated tyrosine phosphosites as identified by LC-MS/MS. T47D and MCF7 parental and resistant cells were treated for 24 hours with respective IC90 concentrations of BYL719 in the presence or absence of insulin in the media. Data are mean ± STD of technical duplicates (n >2, *P <0.05, **P <0.01, ***P ˂0.001). MCF7p MCF7-parental, MCF7r MCF7-resistant, PI3K phosphatidylinositol 3-kinase, T47Dp T47D-parental, T47Dr T47D-resistant