Modeling response to P13K Target Therapies

对 P13K 靶向治疗的反应进行建模

• 批准号: 8181894
• 负责人: GORDON B. MILLS
• 金额: $ 56.25万
• 依托单位: UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2015-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8181894
• 关键词: 1-Phosphatidylinositol 3-Kinase; AKT2 gene; Address; Affect; Apoptosis; BRAF gene; Back; Bioenergetics; Biological; Breast Cancer Cell; Bypass; Cell Cycle Progression; Cell Proliferation; Cell Size; Cell Surface Receptors; Cell physiology; Cereals; Clinical Trials; Complex; Computer Simulation; Data; Development; Drug Combinations; Drug Delivery Systems; Elements; Energy-Generating Resources; Ensure; Epidermal Growth Factor Receptor; Family; Feedback; Generations; Genomics; Glycolysis; Goals; Homeostasis; Imagery; Intervention; Investigation; Knowledge; MEKs; Malignant Neoplasms; Maps; Mediating; Metabolism; Modeling; Molecular; Mutation; Nature; Network-based; Oncogenic; Outcome; PDPK1 gene; PTEN gene; Participant; Pathway interactions; Patients; Pharmaceutical Preparations; Phase; Phosphoproteins; Phosphotransferases; Physiological; Process; Property; Protein Array Analysis; Protein Biosynthesis; Protein Isoforms; Proteins; Proto-Oncogene Proteins c-akt; Series; Signal Pathway; Signal Transduction; Sirolimus; Small Interfering RNA; Source; Structure; System; TSC1 gene; TSC2 gene; Testing; Therapeutic Intervention; Time; Validation; Warburg Effect; base; blood glucose regulation; cell motility; combinatorial; design; feeding; glucose uptake; human FRAP1 protein; inhibitor/antagonist; knock-down; mTOR Inhibitor; malignant breast neoplasm; mathematical model; member; multi-scale modeling; novel; predictive modeling; programs; protein complex; research study; response; stem cell division; therapeutic target; tumor; tumor initiation; tumorigenesis