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Rational, biologically based treatment of EGFR-mutant non-small-cell lung cancer
Open accessAbstract
Epidermal growth factor receptor (EGFR)-mutant non-small-cell lung cancer (NSCLC) was first recognized in 2004 as a distinct, clinically relevant molecular subset of lung cancer. The disease has been the subject of intensive research at both the basic scientific and clinical levels, becoming a paradigm for how to understand and treat oncogene-driven carcinomas. Although patients with EGFR-mutant tumours have increased sensitivity to tyrosine kinase inhibitors (TKIs), primary and acquired resistance to these agents remains a major clinical problem. This Review summarizes recent developments aimed at treating and ultimately curing the disease.
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“The third-generation drug retains the acrylamide group and covalently binds to Cys797, but replaces the quinazoline portion of the first- and second-generation compounds with pyrimidine to promote selectivity for T790M, showing a higher affinity for T790M than WT-EGFR.119”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [119]
In the citing paper
“Mutations in EGFR occur in 10-35% of NSCLCs and confer sensitivity to the EGFR TKIs erlotinib, gefitinib, and afatinib (6).”
From AZD9291, an Irreversible EGFR TKI, Overcomes T790M-Mediated Resistance to EGFR Inhibitors in Lung Cancer (2014) · cites this paper as [6]
In the citing paper
“Exon 20 insertion mutations comprise 4–10% of all EGFR mutations 27,29–32.”
From Structural, Biochemical, and Clinical Characterization of Epidermal Growth Factor Receptor (EGFR) Exon 20 Insertion Mutations in Lung Cancer (2013) · cites this paper as [30]
In the citing paper
“Indeed, while ERBB2 gene amplifications and gain-of-function EGFR mutations support the proliferation of various cancer cell types (Oh and Bang, 2020; Pao and Chmielecki, 2010), VEGFA is critical for tumor-driven neoangiogenesis (Apte et al., 2019) and TGFb promotes the establishment of a fibrotic microenvironment that is poorly permissive to access by therapeutics (Derynck et al., 2020).”
From Immunomodulation by targeted anticancer agents (2021) · cites this paper as Pao and Chmielecki, 2010
In the citing paper
“Over the past two decades, a number of mAbs and TKIs have been developed to target these proteins or their binding partners, and some of these molecules, including HER2-, EGFR-, and VEGFA-specific agents, have been licensed for use in a variety of oncological indications (Apte et al., 2019; Oh and Bang, 2020; Pao and Chmielecki, 2010).”
From Immunomodulation by targeted anticancer agents (2021) · cites this paper as Pao and Chmielecki, 2010
In the citing paper
“EGFR mutations are primarily localized within two hot spots of the kinase domains, a series of overlapping deletions in exon 19 and a leucine to arginine substitution at amino acid position 858 (L858R) [reviewed in (Pao and Chmielecki, 2010)].”
From ERBB Receptors: From Oncogene Discovery to Basic Science to Mechanism-Based Cancer Therapeutics (2014) · cites this paper as Pao and Chmielecki, 2010
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Research works printed but not linked: 1
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“EGFR mutations and the EML4-ALK gene fusion represent two molecular alterations in about 15% of lung adenocarcinoma patients in Western countries, and affect target sites for which drugs are in clinical use (Pao and Chmielecki, 2010).”
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“activation of different pathways by mutations in HGF (hepatocyte growth factor) gene (29), IGF1R (insulin growth factor 1 receptor) gene (30), MET (MET proto-oncogene, receptor tyrosine kinase) gene (31), and/or PI3K/AKT (phosphatidylinositol-3-kinase and protein kinase B) pathway genes (32, 33).”
BackgroundStructural Mechanism and Inhibitors Targeting EGFR Exon 20 Insertion (Ex20ins) Mutations
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“Despite considerable progression in studying lung cancer prevention and treatment, the tumor recurrence with acquired drug resistance frequently occurs in advanced lung cancer [2,3], raising the necessity to understand the biology of lung cancer for a better therapeutic improvement.”
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“Molecular targeted agents that block tumorigenic pathways have been successful in the management of diverse cancer types, such as human epidermal growth factor receptor 2 (HER2)–blocking agents in patients with HER2-positive breast cancer and epidermal growth factor receptor (EGFR)–blocking agents in patients with EGF…”
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“The first and best known example is the discovery of EGFR mutations, characterizing a subgroup of tumors in which the treatment with EGFR selective inhibitors (gefitinib, erlotinib, afatinib) significantly improves survival and quality of life (1-6).”
BackgroundPotent and selective EGFR inhibitors based on 5-aryl-7H-pyrrolopyrimidin-4-amines
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“Routine molecular testing for EGFR mutations or EML4-ALK rearrangements, now a standard practice at our institution and others, have led to personalized medicine approaches using small molecule tyrosine kinase inhibitors (TKI) to elicit responses and improve outcome for lung cancer patients [7].”
BackgroundAnaplastic lymphoma kinase (ALK) mutations in patients with adenocarcinoma of the lung
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“In 2004, the gene was identified as an effective clinical biomarker for the pathogenesis of non-small cell lung cancer [10].”
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“While small molecule tyrosine kinase inhibitors have demonstrated efficacy in several cancers with increased EGFR activity (33, 34), they have been relatively ineffective in GBM (35–37).”
BackgroundChiang, C., Wang, L., Ho, H., Tsai, C., Yeh, Y., Hsu, W., Chou, T., Chiu, C., & Wu, Y. (2017) · Oncotarget · doi:10.18632/oncotarget.23686 · Cited by 13
“Numerous studies showed that in patients with advanced NSCLC carrying EGFR mutations, treatment with epidermal growth factor receptor –tyrosine kinase inhibitors (EGFRTKIs) improved chances of survival [2–6].”
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“However, following a period of treatment with EGFR-TKI, acquired resistances often occur in lung cancer cells [16], which are predominantly due to secondary mutations in EGFR, bypassing the alternative pathway activation or histologic transformation [17].”
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“Among molecular targeted drugs, epithelial growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) have been widely used in NSCLC patients.(6) Studies have shown that EGFR-TKIs are more effective than conventional chemotherapy drugs in NSCLC patients with EGFR sensitive mutation.”
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“The emergence of targeted therapies inhibiting growth factor receptor (GFR), anaplastic lymphoma kinase (ALK), ROS Proto-Oncogene 1 (ROS1), B-raf proto-oncogene (BRAF), and other driver alterations has improved clinical outcomes for NSCLC patients harboring these mutations (6).”
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“Recently, EGFR has been identified as a driver of oncogenes in NSCLC, because the mutation of activating EGFR kinase domain enhances the activity of EGFR tyrosine kinase, leading to continuous activation of the downstream signal pathway, and then drives tumorigenesis and tumor progression (32).”
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Metadata
- Authors
- Pao, W., & Chmielecki, J.
- Affiliations
- Vanderbilt University (US)
- Corresponding author
- Pao, William
- Venue
- Nature Reviews Cancer
- Published
- 2010-10-22
- Volume
- 10
- Issue
- 11
- Pages
- 760-774
- ISSN
- 1474-175X (ISSN-L)
- 1474-1768
- PMC
- PMC3072803
- OpenAlex
- W2090029719
- Cited by
- 1,083
- References
- 180
- Citations by year
- 2026: 24 · 2025: 43 · 2024: 54 · 2023: 49 · 2022: 45 · 2021: 65 · 2020: 79 · 2019: 56 · 2018: 69 · 2017: 72 · 2016: 90 · 2015: 82 · 2014: 93 · 2013: 93 · 2012: 104
- FWCI
- 14.65
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Cancer (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Vanderbilt University
- National Institutes of Health
- University of California, San Francisco
- National Cancer Institute (P30 CA 68485, R01CA121210, P01CA129243, CA90949, U54CA143798, P50CA090949, P30CA068485)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- EGFR-mutant non-small cell lung cancer, epidermal growth factor receptor, tyrosine kinase inhibitors, gefitinib, erlotinib, acquired drug resistance, primary resistance, targeted therapy
- MeSH terms
- Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Humans, Lung Neoplasms, Mutation, Protein-Tyrosine Kinases, Drug Resistance, Neoplasm, Protein Kinase Inhibitors, ErbB Receptors
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