EMT-Mediated Acquired EGFR-TKI Resistance in NSCLC: Mechanisms and Strategies
Acquired resistance inevitably limits the curative effects of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), which represent the classical paradigm of molecular-targeted therapies in non-small-cell lung cancer (NSCLC). How to break such a bottleneck becomes a pressing probl...
Ausführliche Beschreibung
Autor*in: |
Xuan Zhu [verfasserIn] Lijie Chen [verfasserIn] Ling Liu [verfasserIn] Xing Niu [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2019 |
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Übergeordnetes Werk: |
In: Frontiers in Oncology - Frontiers Media S.A., 2012, 9(2019) |
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Übergeordnetes Werk: |
volume:9 ; year:2019 |
Links: |
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DOI / URN: |
10.3389/fonc.2019.01044 |
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DOAJ029582024 |
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10.3389/fonc.2019.01044 doi (DE-627)DOAJ029582024 (DE-599)DOAJ400539dcbd5844bebf29ccc1ca011999 DE-627 ger DE-627 rakwb eng RC254-282 Xuan Zhu verfasserin aut EMT-Mediated Acquired EGFR-TKI Resistance in NSCLC: Mechanisms and Strategies 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Acquired resistance inevitably limits the curative effects of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), which represent the classical paradigm of molecular-targeted therapies in non-small-cell lung cancer (NSCLC). How to break such a bottleneck becomes a pressing problem in cancer treatment. The epithelial-mesenchymal transition (EMT) is a dynamic process that governs biological changes in various aspects of malignancies, notably drug resistance. Progress in delineating the nature of this process offers an opportunity to develop clinical therapeutics to tackle resistance toward anticancer agents. Herein, we seek to provide a framework for the mechanistic underpinnings on the EMT-mediated acquisition of EGFR-TKI resistance, with a focus on NSCLC, and raise the question of what therapeutic strategies along this line should be pursued to optimize the efficacy in clinical practice. epithelial-mesenchymal transition acquired resistance therapeutic strategies non-small-cell lung cancer epidermal growth factor receptor tyrosine kinase inhibitors Neoplasms. Tumors. Oncology. Including cancer and carcinogens Xuan Zhu verfasserin aut Lijie Chen verfasserin aut Ling Liu verfasserin aut Xing Niu verfasserin aut In Frontiers in Oncology Frontiers Media S.A., 2012 9(2019) (DE-627)684965518 (DE-600)2649216-7 2234943X nnns volume:9 year:2019 https://doi.org/10.3389/fonc.2019.01044 kostenfrei https://doaj.org/article/400539dcbd5844bebf29ccc1ca011999 kostenfrei https://www.frontiersin.org/article/10.3389/fonc.2019.01044/full kostenfrei https://doaj.org/toc/2234-943X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2019 |
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10.3389/fonc.2019.01044 doi (DE-627)DOAJ029582024 (DE-599)DOAJ400539dcbd5844bebf29ccc1ca011999 DE-627 ger DE-627 rakwb eng RC254-282 Xuan Zhu verfasserin aut EMT-Mediated Acquired EGFR-TKI Resistance in NSCLC: Mechanisms and Strategies 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Acquired resistance inevitably limits the curative effects of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), which represent the classical paradigm of molecular-targeted therapies in non-small-cell lung cancer (NSCLC). How to break such a bottleneck becomes a pressing problem in cancer treatment. The epithelial-mesenchymal transition (EMT) is a dynamic process that governs biological changes in various aspects of malignancies, notably drug resistance. Progress in delineating the nature of this process offers an opportunity to develop clinical therapeutics to tackle resistance toward anticancer agents. Herein, we seek to provide a framework for the mechanistic underpinnings on the EMT-mediated acquisition of EGFR-TKI resistance, with a focus on NSCLC, and raise the question of what therapeutic strategies along this line should be pursued to optimize the efficacy in clinical practice. epithelial-mesenchymal transition acquired resistance therapeutic strategies non-small-cell lung cancer epidermal growth factor receptor tyrosine kinase inhibitors Neoplasms. Tumors. Oncology. Including cancer and carcinogens Xuan Zhu verfasserin aut Lijie Chen verfasserin aut Ling Liu verfasserin aut Xing Niu verfasserin aut In Frontiers in Oncology Frontiers Media S.A., 2012 9(2019) (DE-627)684965518 (DE-600)2649216-7 2234943X nnns volume:9 year:2019 https://doi.org/10.3389/fonc.2019.01044 kostenfrei https://doaj.org/article/400539dcbd5844bebf29ccc1ca011999 kostenfrei https://www.frontiersin.org/article/10.3389/fonc.2019.01044/full kostenfrei https://doaj.org/toc/2234-943X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2019 |
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RC254-282 EMT-Mediated Acquired EGFR-TKI Resistance in NSCLC: Mechanisms and Strategies epithelial-mesenchymal transition acquired resistance therapeutic strategies non-small-cell lung cancer epidermal growth factor receptor tyrosine kinase inhibitors |
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EMT-Mediated Acquired EGFR-TKI Resistance in NSCLC: Mechanisms and Strategies |
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Acquired resistance inevitably limits the curative effects of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), which represent the classical paradigm of molecular-targeted therapies in non-small-cell lung cancer (NSCLC). How to break such a bottleneck becomes a pressing problem in cancer treatment. The epithelial-mesenchymal transition (EMT) is a dynamic process that governs biological changes in various aspects of malignancies, notably drug resistance. Progress in delineating the nature of this process offers an opportunity to develop clinical therapeutics to tackle resistance toward anticancer agents. Herein, we seek to provide a framework for the mechanistic underpinnings on the EMT-mediated acquisition of EGFR-TKI resistance, with a focus on NSCLC, and raise the question of what therapeutic strategies along this line should be pursued to optimize the efficacy in clinical practice. |
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Acquired resistance inevitably limits the curative effects of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), which represent the classical paradigm of molecular-targeted therapies in non-small-cell lung cancer (NSCLC). How to break such a bottleneck becomes a pressing problem in cancer treatment. The epithelial-mesenchymal transition (EMT) is a dynamic process that governs biological changes in various aspects of malignancies, notably drug resistance. Progress in delineating the nature of this process offers an opportunity to develop clinical therapeutics to tackle resistance toward anticancer agents. Herein, we seek to provide a framework for the mechanistic underpinnings on the EMT-mediated acquisition of EGFR-TKI resistance, with a focus on NSCLC, and raise the question of what therapeutic strategies along this line should be pursued to optimize the efficacy in clinical practice. |
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Acquired resistance inevitably limits the curative effects of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs), which represent the classical paradigm of molecular-targeted therapies in non-small-cell lung cancer (NSCLC). How to break such a bottleneck becomes a pressing problem in cancer treatment. The epithelial-mesenchymal transition (EMT) is a dynamic process that governs biological changes in various aspects of malignancies, notably drug resistance. Progress in delineating the nature of this process offers an opportunity to develop clinical therapeutics to tackle resistance toward anticancer agents. Herein, we seek to provide a framework for the mechanistic underpinnings on the EMT-mediated acquisition of EGFR-TKI resistance, with a focus on NSCLC, and raise the question of what therapeutic strategies along this line should be pursued to optimize the efficacy in clinical practice. |
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score |
7.4009714 |