The current version of this model includes more than 4,700 intracellular biolog

These data represent supplier Amuvatinib viability as mean values from triplicate samples. We tested ten anti cancer drugs in silico on the simu lation avatars of the 8 patient derived GBM cell lines in a blinded prospective study. These simulations generated predictions that we compared with in vitro experimental data. Of the 80 in silico predictions, 61 predictions showed agreement with in vitro experimental results. Analysis of drug sensitivity correlation for all 8 GBM patient derived cell lines, for all the 13 drugs is summarized in Additional file 1Table S7. Figures 5A H and 6A H show a drug wise comparison of in silico predictions and in vitro experimental results generated with testing 1 uM concentration of each drug on these cell lines.<br><br> Effect of tyrosine kinase inhibitors on patient derived AT-406 価格 GBM cells For the EGFR family inhibitor lapatinib, simulation stud ies predicted SK429, SK748 and SK1035 to be resistant, which were confirmed by in vitro data. Similarly, model ing predicted GBM8, SK102, SK262 and SK987 to be sensitive and these predictions were in agreement with experimental data. However, modeling predicted GBM4 to be resistant to lapatinib while in vitro data showed GBM4 to be highly sensitive to lapatinib. For the tyrosine kinase inhibitor nilotinib, the model predicted GBM8 to be sensitive while all the other profiles to be resistant. In vitro stud ies demonstrated that GBM8 was indeed sensitive to nilotinib as predicted, but there was a mismatch with the experimental results for two lines SK262 and SK1035. Experimentally, SK262 was found to be sensi tive, whereas SK1035 was on the borderline of sensitiv ity and resistance.<br><br> For imatinib, simulation predicted that all GBM lines except GBM8 were resist ant. The experimental results corroborated with this in silico prediction. Sunitinib was supplier AG-490 the other multi tyrosine kinase inhibitor tested. Our simulation predicted GBM8, SK102 and SK987 to be sensitive to sunitinib. however, only GBM8 was found to be sensitive in vitro. SK262 was predicted to be re sistant to sunitinib but in vitro data found it to be moder ately sensitive. On the other hand, GBM4, SK429, SK748 and SK1035 were found to be resistant in both simulation and experimental data. Effect of other drugs on patient derived GBM cells Besides the tyrosine kinase inhibitors, correlation be tween in silico predictions and experimental results for the 8 patient derived GBM cell lines was also tested for drugs such as pitavastatin, everolimus, celecoxib and bortezomib.<br><br> For bortezomib, all profiles were predicted to be sensitive and these predictions matched with in vitro ex perimental results. For everolimus, in vitro results were in agreement with simulation pre dictions for all lines except SK429. Our in silico model predicted GBM4, SK262, SK429, SK748 and SK1035 to be resistant to celecoxib. these pre dictions matched with in vitro results. However, GBM8, SK102 and SK987 were predicted to show moderate sensi tivity to celecoxib, but were found to be resistant in vitro. For pitavastatin, the simulation pre dicted 5 patient derived GBM cell lines to be sensitive, of which SK987 was found to be resistant in vitro.