{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang XY"],"funding":["NCI NIH HHS","NIGMS NIH HHS"],"pagination":["e92"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3910016"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["3"],"pubmed_abstract":["A unified approach to optimize multidrug chemotherapy using a pharmacokinetic (PK)/enhanced pharmacodynamic model was developed using the vascular endothelial growth factor receptor (VEGFR) signaling system. The base VEGFR network model, characterized by ligand-receptor interactions, enzyme recruitment (Grb2-Sos, phospholipase C γ (PLCγ), and phosphoinositide-3 kinase (PI3K)), and downstream mitogen-activated protein kinase and Akt cascade activation, was linked to a sunitinib (VEGFR inhibitor) PK model and underwent Sobol sensitivity analysis that revealed potential sunitinib-enhancing mechanisms. Drugs targeting these mechanisms (a VEGF inhibitor, a PI3K inhibitor, a PLCγ inhibitor, and a mitogen-activated protein kinase inhibitor) and sunitinib were input to optimization-based control a"],"journal":["CPT: pharmacometrics & systems pharmacology"],"pubmed_title":["A General Network Pharmacodynamic Model-Based Design Pipeline for Customized Cancer Therapy Applied to the VEGFR Pathway."],"pmcid":["PMC3910016"],"funding_grant_id":["P50 GM071558","R01 CA127963","R01 CA072937"],"pubmed_authors":["Zhang XY","Birtwistle MR","Gallo JM"],"additional_accession":[]},"is_claimable":false,"name":"A General Network Pharmacodynamic Model-Based Design Pipeline for Customized Cancer Therapy Applied to the VEGFR Pathway.","description":"A unified approach to optimize multidrug chemotherapy using a pharmacokinetic (PK)/enhanced pharmacodynamic model was developed using the vascular endothelial growth factor receptor (VEGFR) signaling system. The base VEGFR network model, characterized by ligand-receptor interactions, enzyme recruitment (Grb2-Sos, phospholipase C γ (PLCγ), and phosphoinositide-3 kinase (PI3K)), and downstream mitogen-activated protein kinase and Akt cascade activation, was linked to a sunitinib (VEGFR inhibitor) PK model and underwent Sobol sensitivity analysis that revealed potential sunitinib-enhancing mechanisms. Drugs targeting these mechanisms (a VEGF inhibitor, a PI3K inhibitor, a PLCγ inhibitor, and a mitogen-activated protein kinase inhibitor) and sunitinib were input to optimization-based control a","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Jan","modification":"2025-05-18T11:15:59.009Z","creation":"2025-05-18T11:15:59.009Z"},"accession":"S-EPMC3910016","cross_references":{"pubmed":["24429593"],"doi":["10.1038/psp.2013.65"]}}