Targeting Epidermal Growth Factor Receptor in Non-Small-Cell-Lung Cancer : Current State and Future Perspective
Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net..
BACKGROUND: Lung cancer is one of the leading cause of cancer death worldwide, the most common histological type of lung cancer is non-small cell lung cancer (NSCLC), whose occurrence and development is closely related to the mutation and amplification of epidermal growth factor receptors (EGFR). Currently , a series of targeted drugs were developed on the inhibition of EGFR such as epidermal growth factor receptortyrosine kinase inhibitor EGFR-TKI and monoclonal antibody (McAb).
OBJECTIVE: We sought to summarizes the current drugs targeting Epidermal Growth Factor Receptor in nonsmall- cell-lung.
METHODS: We conducted a comprehensive review of the development and application of EGFR-TKI and McAb which targeted EGFR in NSCLC and compared the mechanisms of PROTAC with the traditional inhibitors.
RESULTS: The drugs targeted EGFR in NSCLC have been widely used in clinic practices. Compared to traditional chemotherapy, these drugs excel with their clear and specific targeting, better curative effects, and less toxic and side effects. However, the mechanism comes with some insurmountable weaknesses like serious toxic and other side effects, as well as proneness to producing drug resistance.
CONCLUSION: The emerging PROTAC (Proteolysis Targeting Chimera) technology has been successfully applied to selective degradation of multiple protein targets, including EGFR. It also highlights the potential and challenges of PROTAC therapy regarding future combination therapeutic options in NSCLC treatment.
Medienart: |
E-Artikel |
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Erscheinungsjahr: |
2019 |
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Erschienen: |
2019 |
Enthalten in: |
Zur Gesamtaufnahme - volume:19 |
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Enthalten in: |
Anti-cancer agents in medicinal chemistry - 19(2019), 8 vom: 10., Seite 984-991 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Bao, Shui-Ming [VerfasserIn] |
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Links: |
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Themen: |
Antineoplastic Agents |
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Anmerkungen: |
Date Completed 24.03.2020 Date Revised 24.03.2020 published: Print Citation Status MEDLINE |
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doi: |
10.2174/1871520619666190313161009 |
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funding: |
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Förderinstitution / Projekttitel: |
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PPN (Katalog-ID): |
NLM294920994 |
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520 | |a Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net. | ||
520 | |a BACKGROUND: Lung cancer is one of the leading cause of cancer death worldwide, the most common histological type of lung cancer is non-small cell lung cancer (NSCLC), whose occurrence and development is closely related to the mutation and amplification of epidermal growth factor receptors (EGFR). Currently , a series of targeted drugs were developed on the inhibition of EGFR such as epidermal growth factor receptortyrosine kinase inhibitor EGFR-TKI and monoclonal antibody (McAb) | ||
520 | |a OBJECTIVE: We sought to summarizes the current drugs targeting Epidermal Growth Factor Receptor in nonsmall- cell-lung | ||
520 | |a METHODS: We conducted a comprehensive review of the development and application of EGFR-TKI and McAb which targeted EGFR in NSCLC and compared the mechanisms of PROTAC with the traditional inhibitors | ||
520 | |a RESULTS: The drugs targeted EGFR in NSCLC have been widely used in clinic practices. Compared to traditional chemotherapy, these drugs excel with their clear and specific targeting, better curative effects, and less toxic and side effects. However, the mechanism comes with some insurmountable weaknesses like serious toxic and other side effects, as well as proneness to producing drug resistance | ||
520 | |a CONCLUSION: The emerging PROTAC (Proteolysis Targeting Chimera) technology has been successfully applied to selective degradation of multiple protein targets, including EGFR. It also highlights the potential and challenges of PROTAC therapy regarding future combination therapeutic options in NSCLC treatment | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Research Support, Non-U.S. Gov't | |
650 | 4 | |a Review | |
650 | 4 | |a EGFR-TKls | |
650 | 4 | |a McAb | |
650 | 4 | |a NSCLC | |
650 | 4 | |a PROTAC | |
650 | 4 | |a protein degradation | |
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700 | 1 | |a Tong, Yin-Ping |e verfasserin |4 aut | |
700 | 1 | |a Bao, Wen-Dai |e verfasserin |4 aut | |
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