Contribution of EGFR and ErbB-3 heterodimerization to the EGFR mutation-induced gefitinib- and erlotinib-resistance in non-small-cell lung carcinoma treatments

• المؤلفون الرئيسيون: Wang D.D., Ma L., Wong M.P., Lee V.H.F., Yan H.
• مؤلفون آخرون: SAW SWEE HOCK SCHOOL OF PUBLIC HEALTH
• التنسيق: مقال
• منشور في: 2019
• الموضوعات: epidermal growth factor receptor; epidermal growth factor receptor 2; epidermal growth factor receptor 3; erlotinib; gefitinib; scatter factor receptor; somatomedin C receptor; ERBB3 protein, human; mutant protein; protein binding; protein kinase inhibitor; quinazoline derivative; Article; binding affinity; dimerization; female; gene deletion; heterodimerization; human; major clinical study; male; mutation; non small cell lung cancer; progression free survival; protein function; protein protein interaction; signal transduction; Carcinoma, Non-Small-Cell Lung; chemistry; disease free survival; drug effects; drug resistance; genetics; Lung Neoplasms; metabolism; molecular dynamics; protein multimerization; regression analysis; structural homology; thermodynamics; Disease-Free Survival; Drug Resistance, Neoplasm; Erlotinib Hydrochloride; Humans; Molecular Dynamics Simulation; Mutant Proteins; Mutation; Protein Binding; Protein Kinase Inhibitors; Protein Multimerization; Quinazolines; Receptor, Epidermal Growth Factor; Receptor, ErbB-3; Regression Analysis; Signal Transduction; Structural Homology, Protein; Thermodynamics
• الوصول للمادة أونلاين: https://scholarbank.nus.edu.sg/handle/10635/161510
• المؤسسة: National University of Singapore

10.1371/journal.pone.0128360