Drug resistance of targeted therapy for advanced non-small cell lung cancer harbored EGFR mutation: from mechanism analysis to clinical strategy

Purpose Non-small cell lung cancer (NSCLC) accounts for about 85% in all cases of lung cancer. In recent years, molecular targeting drugs for NSCLC have been developed rapidly. The epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have changed the paradigm of cancer therapy fro...

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Published inJournal of cancer research and clinical oncology Vol. 147; no. 12; pp. 3653 - 3664
Main Authors Zhao, Yuxin, Wang, Haiyong, He, Chengwei
Format Journal Article
LanguageEnglish
Published Berlin/Heidelberg Springer Berlin Heidelberg 01.12.2021
Springer Nature B.V
Subjects
Antineoplastic Agents - therapeutic use
c-Met protein
Cancer Research
Cancer therapies
Carcinoma, Non-Small-Cell Lung - drug therapy
Carcinoma, Non-Small-Cell Lung - genetics
Chemotherapy
Cytotoxicity
Drug delivery
Drug resistance
Drug Resistance, Neoplasm - physiology
Epidermal growth factor
Epidermal growth factor receptors
ErbB protein
ErbB Receptors - antagonists & inhibitors
ErbB Receptors - genetics
ErbB-2 protein
Hematology
Hepatocyte growth factor
Humans
Insulin
Insulin-like growth factor I
Internal Medicine
Lung cancer
Lung Neoplasms - drug therapy
Lung Neoplasms - genetics
Medicine
Medicine & Public Health
Mesenchyme
Molecular Targeted Therapy - methods
Mutation
Non-small cell lung carcinoma
Oncology
Protein Kinase Inhibitors - therapeutic use
Protein-tyrosine kinase
PTEN protein
Review – Clinical Oncology
Small cell lung carcinoma
Stat3 protein
Tensin
Transcription activation
Tumors
Vascular endothelial growth factor
Drug resistance
Targeted therapy
Non-small cell lung cancer
Epidermal growth factor receptor-tyrosine kinase inhibitor
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Abstract Purpose Non-small cell lung cancer (NSCLC) accounts for about 85% in all cases of lung cancer. In recent years, molecular targeting drugs for NSCLC have been developed rapidly. The epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have changed the paradigm of cancer therapy from empirical cytotoxic chemotherapy to molecular-targeted cancer therapy. Currently, there are three generations of EGFR-TKIs, all of which have achieved good efficacy in clinical therapy. However, most patients developed drug resistance after 6–13 months EGFR-TKIs treatment. Therefore, a comprehensive understanding of EGFR-TKIs resistance mechanisms is of vital importance for clinical management of NSCLC. Methods Relevant data and information about the topic were obtained by searching PubMed (Medline), Web of Science and Google Scholar using the subject headings, such as “NSCLC”, “EGFR-TKIs resistance”, “EGFR mutations”, “human epidermal growth factor receptor-2 (HER2/erbB-2)”, “hepatocyte growth factor (HGF)”, “vascular endothelial growth factor (VEGF)”, “insulin-like growth factor 1 (IGF-1)”, “epithelial–mesenchymal transition (EMT)”, “phosphatase and tensin homolog (PTEN)”, “RAS mutation”, “BRAF mutation”, “signal transducer and activator of transcription 3 (STAT3)”, and “tumor microenvironment”, etc. Results The mechanisms for EGFR-TKIs resistance include EGFR mutations, upregulation of HER2, HGF/c-MET, VEGF IGF1, EMT and STAT3 pathways, mutations of PTEN, RAS and BRAF genes, and activation of other by-pass pathways. These mechanisms are interconnected and can be potential targets for the treatment of NSCLC. Conclusion In this review, we discuss the mechanisms of EGFR-TKIs drug resistance and the clinical strategies to overcome drug resistance from the perspective of EGFR-TKIs combined treatment.
AbstractList Non-small cell lung cancer (NSCLC) accounts for about 85% in all cases of lung cancer. In recent years, molecular targeting drugs for NSCLC have been developed rapidly. The epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have changed the paradigm of cancer therapy from empirical cytotoxic chemotherapy to molecular-targeted cancer therapy. Currently, there are three generations of EGFR-TKIs, all of which have achieved good efficacy in clinical therapy. However, most patients developed drug resistance after 6-13 months EGFR-TKIs treatment. Therefore, a comprehensive understanding of EGFR-TKIs resistance mechanisms is of vital importance for clinical management of NSCLC. Relevant data and information about the topic were obtained by searching PubMed (Medline), Web of Science and Google Scholar using the subject headings, such as "NSCLC", "EGFR-TKIs resistance", "EGFR mutations", "human epidermal growth factor receptor-2 (HER2/erbB-2)", "hepatocyte growth factor (HGF)", "vascular endothelial growth factor (VEGF)", "insulin-like growth factor 1 (IGF-1)", "epithelial-mesenchymal transition (EMT)", "phosphatase and tensin homolog (PTEN)", "RAS mutation", "BRAF mutation", "signal transducer and activator of transcription 3 (STAT3)", and "tumor microenvironment", etc. RESULTS: The mechanisms for EGFR-TKIs resistance include EGFR mutations, upregulation of HER2, HGF/c-MET, VEGF IGF1, EMT and STAT3 pathways, mutations of PTEN, RAS and BRAF genes, and activation of other by-pass pathways. These mechanisms are interconnected and can be potential targets for the treatment of NSCLC. In this review, we discuss the mechanisms of EGFR-TKIs drug resistance and the clinical strategies to overcome drug resistance from the perspective of EGFR-TKIs combined treatment.
PurposeNon-small cell lung cancer (NSCLC) accounts for about 85% in all cases of lung cancer. In recent years, molecular targeting drugs for NSCLC have been developed rapidly. The epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have changed the paradigm of cancer therapy from empirical cytotoxic chemotherapy to molecular-targeted cancer therapy. Currently, there are three generations of EGFR-TKIs, all of which have achieved good efficacy in clinical therapy. However, most patients developed drug resistance after 6–13 months EGFR-TKIs treatment. Therefore, a comprehensive understanding of EGFR-TKIs resistance mechanisms is of vital importance for clinical management of NSCLC.MethodsRelevant data and information about the topic were obtained by searching PubMed (Medline), Web of Science and Google Scholar using the subject headings, such as “NSCLC”, “EGFR-TKIs resistance”, “EGFR mutations”, “human epidermal growth factor receptor-2 (HER2/erbB-2)”, “hepatocyte growth factor (HGF)”, “vascular endothelial growth factor (VEGF)”, “insulin-like growth factor 1 (IGF-1)”, “epithelial–mesenchymal transition (EMT)”, “phosphatase and tensin homolog (PTEN)”, “RAS mutation”, “BRAF mutation”, “signal transducer and activator of transcription 3 (STAT3)”, and “tumor microenvironment”, etc.ResultsThe mechanisms for EGFR-TKIs resistance include EGFR mutations, upregulation of HER2, HGF/c-MET, VEGF IGF1, EMT and STAT3 pathways, mutations of PTEN, RAS and BRAF genes, and activation of other by-pass pathways. These mechanisms are interconnected and can be potential targets for the treatment of NSCLC.ConclusionIn this review, we discuss the mechanisms of EGFR-TKIs drug resistance and the clinical strategies to overcome drug resistance from the perspective of EGFR-TKIs combined treatment.
Purpose Non-small cell lung cancer (NSCLC) accounts for about 85% in all cases of lung cancer. In recent years, molecular targeting drugs for NSCLC have been developed rapidly. The epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have changed the paradigm of cancer therapy from empirical cytotoxic chemotherapy to molecular-targeted cancer therapy. Currently, there are three generations of EGFR-TKIs, all of which have achieved good efficacy in clinical therapy. However, most patients developed drug resistance after 6–13 months EGFR-TKIs treatment. Therefore, a comprehensive understanding of EGFR-TKIs resistance mechanisms is of vital importance for clinical management of NSCLC. Methods Relevant data and information about the topic were obtained by searching PubMed (Medline), Web of Science and Google Scholar using the subject headings, such as “NSCLC”, “EGFR-TKIs resistance”, “EGFR mutations”, “human epidermal growth factor receptor-2 (HER2/erbB-2)”, “hepatocyte growth factor (HGF)”, “vascular endothelial growth factor (VEGF)”, “insulin-like growth factor 1 (IGF-1)”, “epithelial–mesenchymal transition (EMT)”, “phosphatase and tensin homolog (PTEN)”, “RAS mutation”, “BRAF mutation”, “signal transducer and activator of transcription 3 (STAT3)”, and “tumor microenvironment”, etc. Results The mechanisms for EGFR-TKIs resistance include EGFR mutations, upregulation of HER2, HGF/c-MET, VEGF IGF1, EMT and STAT3 pathways, mutations of PTEN, RAS and BRAF genes, and activation of other by-pass pathways. These mechanisms are interconnected and can be potential targets for the treatment of NSCLC. Conclusion In this review, we discuss the mechanisms of EGFR-TKIs drug resistance and the clinical strategies to overcome drug resistance from the perspective of EGFR-TKIs combined treatment.
Non-small cell lung cancer (NSCLC) accounts for about 85% in all cases of lung cancer. In recent years, molecular targeting drugs for NSCLC have been developed rapidly. The epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have changed the paradigm of cancer therapy from empirical cytotoxic chemotherapy to molecular-targeted cancer therapy. Currently, there are three generations of EGFR-TKIs, all of which have achieved good efficacy in clinical therapy. However, most patients developed drug resistance after 6-13 months EGFR-TKIs treatment. Therefore, a comprehensive understanding of EGFR-TKIs resistance mechanisms is of vital importance for clinical management of NSCLC.PURPOSENon-small cell lung cancer (NSCLC) accounts for about 85% in all cases of lung cancer. In recent years, molecular targeting drugs for NSCLC have been developed rapidly. The epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have changed the paradigm of cancer therapy from empirical cytotoxic chemotherapy to molecular-targeted cancer therapy. Currently, there are three generations of EGFR-TKIs, all of which have achieved good efficacy in clinical therapy. However, most patients developed drug resistance after 6-13 months EGFR-TKIs treatment. Therefore, a comprehensive understanding of EGFR-TKIs resistance mechanisms is of vital importance for clinical management of NSCLC.Relevant data and information about the topic were obtained by searching PubMed (Medline), Web of Science and Google Scholar using the subject headings, such as "NSCLC", "EGFR-TKIs resistance", "EGFR mutations", "human epidermal growth factor receptor-2 (HER2/erbB-2)", "hepatocyte growth factor (HGF)", "vascular endothelial growth factor (VEGF)", "insulin-like growth factor 1 (IGF-1)", "epithelial-mesenchymal transition (EMT)", "phosphatase and tensin homolog (PTEN)", "RAS mutation", "BRAF mutation", "signal transducer and activator of transcription 3 (STAT3)", and "tumor microenvironment", etc. RESULTS: The mechanisms for EGFR-TKIs resistance include EGFR mutations, upregulation of HER2, HGF/c-MET, VEGF IGF1, EMT and STAT3 pathways, mutations of PTEN, RAS and BRAF genes, and activation of other by-pass pathways. These mechanisms are interconnected and can be potential targets for the treatment of NSCLC.METHODSRelevant data and information about the topic were obtained by searching PubMed (Medline), Web of Science and Google Scholar using the subject headings, such as "NSCLC", "EGFR-TKIs resistance", "EGFR mutations", "human epidermal growth factor receptor-2 (HER2/erbB-2)", "hepatocyte growth factor (HGF)", "vascular endothelial growth factor (VEGF)", "insulin-like growth factor 1 (IGF-1)", "epithelial-mesenchymal transition (EMT)", "phosphatase and tensin homolog (PTEN)", "RAS mutation", "BRAF mutation", "signal transducer and activator of transcription 3 (STAT3)", and "tumor microenvironment", etc. RESULTS: The mechanisms for EGFR-TKIs resistance include EGFR mutations, upregulation of HER2, HGF/c-MET, VEGF IGF1, EMT and STAT3 pathways, mutations of PTEN, RAS and BRAF genes, and activation of other by-pass pathways. These mechanisms are interconnected and can be potential targets for the treatment of NSCLC.In this review, we discuss the mechanisms of EGFR-TKIs drug resistance and the clinical strategies to overcome drug resistance from the perspective of EGFR-TKIs combined treatment.CONCLUSIONIn this review, we discuss the mechanisms of EGFR-TKIs drug resistance and the clinical strategies to overcome drug resistance from the perspective of EGFR-TKIs combined treatment.
Author Zhao, Yuxin
He, Chengwei
Wang, Haiyong
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  organization: State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Department of Pharmaceutical Science, University of Macau, Guangdong-Hong Kong-Macau Joint Lab on Chinese Medicine and Immune Disease Research, University of Macau
BackLink https://www.ncbi.nlm.nih.gov/pubmed/34661758$$D View this record in MEDLINE/PubMed
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2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
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Issue 12
Keywords Drug resistance
Targeted therapy
Non-small cell lung cancer
Epidermal growth factor receptor-tyrosine kinase inhibitor
Language English
License 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
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Snippet Purpose Non-small cell lung cancer (NSCLC) accounts for about 85% in all cases of lung cancer. In recent years, molecular targeting drugs for NSCLC have been...
Non-small cell lung cancer (NSCLC) accounts for about 85% in all cases of lung cancer. In recent years, molecular targeting drugs for NSCLC have been developed...
PurposeNon-small cell lung cancer (NSCLC) accounts for about 85% in all cases of lung cancer. In recent years, molecular targeting drugs for NSCLC have been...
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SubjectTerms Antineoplastic Agents - therapeutic use
c-Met protein
Cancer Research
Cancer therapies
Carcinoma, Non-Small-Cell Lung - drug therapy
Carcinoma, Non-Small-Cell Lung - genetics
Chemotherapy
Cytotoxicity
Drug delivery
Drug resistance
Drug Resistance, Neoplasm - physiology
Epidermal growth factor
Epidermal growth factor receptors
ErbB protein
ErbB Receptors - antagonists & inhibitors
ErbB Receptors - genetics
ErbB-2 protein
Hematology
Hepatocyte growth factor
Humans
Insulin
Insulin-like growth factor I
Internal Medicine
Lung cancer
Lung Neoplasms - drug therapy
Lung Neoplasms - genetics
Medicine
Medicine & Public Health
Mesenchyme
Molecular Targeted Therapy - methods
Mutation
Non-small cell lung carcinoma
Oncology
Protein Kinase Inhibitors - therapeutic use
Protein-tyrosine kinase
PTEN protein
Review – Clinical Oncology
Small cell lung carcinoma
Stat3 protein
Tensin
Transcription activation
Tumors
Vascular endothelial growth factor
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Title Drug resistance of targeted therapy for advanced non-small cell lung cancer harbored EGFR mutation: from mechanism analysis to clinical strategy
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