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

10.1371/journal.pone.0128360

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Main Authors:	Wang D.D., Ma L., Wong M.P., Lee V.H.F., Yan H.
Other Authors:	SAW SWEE HOCK SCHOOL OF PUBLIC HEALTH
Format:	Article
Published:	2019
Subjects:	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
Online Access:	https://scholarbank.nus.edu.sg/handle/10635/161510
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Institution:	National University of Singapore

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spelling	sg-nus-scholar.10635-1615102023-08-29T22:19:38Z Contribution of EGFR and ErbB-3 heterodimerization to the EGFR mutation-induced gefitinib- and erlotinib-resistance in non-small-cell lung carcinoma treatments Wang D.D. Ma L. Wong M.P. Lee V.H.F. Yan H. SAW SWEE HOCK SCHOOL OF PUBLIC HEALTH epidermal growth factor receptor epidermal growth factor receptor 2 epidermal growth factor receptor 3 erlotinib gefitinib scatter factor receptor somatomedin C receptor epidermal growth factor receptor epidermal growth factor receptor 3 ERBB3 protein, human erlotinib gefitinib 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 mutation protein multimerization regression analysis structural homology thermodynamics Carcinoma, Non-Small-Cell Lung Disease-Free Survival Drug Resistance, Neoplasm Erlotinib Hydrochloride Humans Lung Neoplasms 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 10.1371/journal.pone.0128360 PLoS ONE 10 5 e0128360 2019-11-06T01:30:36Z 2019-11-06T01:30:36Z 2015 Article Wang D.D., Ma L., Wong M.P., Lee V.H.F., Yan H. (2015). Contribution of EGFR and ErbB-3 heterodimerization to the EGFR mutation-induced gefitinib- and erlotinib-resistance in non-small-cell lung carcinoma treatments. PLoS ONE 10 (5) : e0128360. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0128360 19326203 https://scholarbank.nus.edu.sg/handle/10635/161510 Attribution 4.0 International http://creativecommons.org/licenses/by/4.0/ Unpaywall 20191101
institution	National University of Singapore
building	NUS Library
continent	Asia
country	Singapore Singapore
content_provider	NUS Library
collection	ScholarBank@NUS
topic	epidermal growth factor receptor epidermal growth factor receptor 2 epidermal growth factor receptor 3 erlotinib gefitinib scatter factor receptor somatomedin C receptor epidermal growth factor receptor epidermal growth factor receptor 3 ERBB3 protein, human erlotinib gefitinib 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 mutation protein multimerization regression analysis structural homology thermodynamics Carcinoma, Non-Small-Cell Lung Disease-Free Survival Drug Resistance, Neoplasm Erlotinib Hydrochloride Humans Lung Neoplasms 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
spellingShingle	epidermal growth factor receptor epidermal growth factor receptor 2 epidermal growth factor receptor 3 erlotinib gefitinib scatter factor receptor somatomedin C receptor epidermal growth factor receptor epidermal growth factor receptor 3 ERBB3 protein, human erlotinib gefitinib 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 mutation protein multimerization regression analysis structural homology thermodynamics Carcinoma, Non-Small-Cell Lung Disease-Free Survival Drug Resistance, Neoplasm Erlotinib Hydrochloride Humans Lung Neoplasms 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 Wang D.D. Ma L. Wong M.P. Lee V.H.F. Yan H. Contribution of EGFR and ErbB-3 heterodimerization to the EGFR mutation-induced gefitinib- and erlotinib-resistance in non-small-cell lung carcinoma treatments
description	10.1371/journal.pone.0128360
author2	SAW SWEE HOCK SCHOOL OF PUBLIC HEALTH
author_facet	SAW SWEE HOCK SCHOOL OF PUBLIC HEALTH Wang D.D. Ma L. Wong M.P. Lee V.H.F. Yan H.
format	Article
author	Wang D.D. Ma L. Wong M.P. Lee V.H.F. Yan H.
author_sort	Wang D.D.
title	Contribution of EGFR and ErbB-3 heterodimerization to the EGFR mutation-induced gefitinib- and erlotinib-resistance in non-small-cell lung carcinoma treatments
title_short	Contribution of EGFR and ErbB-3 heterodimerization to the EGFR mutation-induced gefitinib- and erlotinib-resistance in non-small-cell lung carcinoma treatments
title_full	Contribution of EGFR and ErbB-3 heterodimerization to the EGFR mutation-induced gefitinib- and erlotinib-resistance in non-small-cell lung carcinoma treatments
title_fullStr	Contribution of EGFR and ErbB-3 heterodimerization to the EGFR mutation-induced gefitinib- and erlotinib-resistance in non-small-cell lung carcinoma treatments
title_full_unstemmed	Contribution of EGFR and ErbB-3 heterodimerization to the EGFR mutation-induced gefitinib- and erlotinib-resistance in non-small-cell lung carcinoma treatments
title_sort	contribution of egfr and erbb-3 heterodimerization to the egfr mutation-induced gefitinib- and erlotinib-resistance in non-small-cell lung carcinoma treatments
publishDate	2019
url	https://scholarbank.nus.edu.sg/handle/10635/161510
_version_	1778169205544189952

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

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