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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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“exon 20, the L748S and D761Y point mutations in exon 19, and the T853A point mutation in exon 21 [16,23], and these”
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“57 In our study, the allele frequency distribution in the metastasis group ranged from 1.62% to 35.42% with a predominance of 16, 18, and 20 CA repeats, whereas in the nonmetastasis group it ranged from 1.42% to 39.15%, with the same pre-dominance of 16, 18, and 20 CA repeats.”
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“epidermal growth factor receptor (EGFR) provided alternative strategies for treating this disease [1].”
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“Caspase proteins comprise a large family that among its initiator proteins, the most notable ones are caspase proteins 2, 8, 9, and 10 (Pop and Salvesen 2009).”
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“Various targeted therapies have been developed to inhibit EGFR signaling in cancer (4).”
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“While the activity of TKIs in NSCLC is essentially restricted to the minority of tumors which carry activating kinase domain mutations of EGFR, the antitumor activity of EGFR monoclonal antibodies such as cetuximab appears to be independent of EGFRmutation status [11–15].”
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“and is divided into three main types, including adenocarcinoma, squamous cell carcinoma, and large-cell carcinoma.(2) Resistance to anticancer agents is a significant problem and is observed frequently in the treatment of patients with smallcell lung cancer and nonesmall-cell lung cancer.”
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“Therapeutic advances in treatment of lung cancer have included targeted therapies, which are available for patients with mutations in oncogenes such as ROS Proto-Oncogene 1 (ROS1), epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), and B-raf proto-oncogene (BRAF) [5–8].”
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“They can make a covalent bond with C797 residue of the EGFR [3].”
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“A detailed discussion on other mechanisms of resistance to EGFR inhibitors is beyond the scope of this article, but the reader is directed to these excellent reviews [6,16].”
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“Signi fi cantly, using SOS1 degraders could prevent the effects caused bypotentialsecondarymutationsthatemergeasacquiredresistancetoRTK-RAS-MAPKpathwayinhibitorsthatresultinpathwayreacti-vation, as observed with targeted therapies in EGFR - and KRAS - mutant tumors (6, 53 – 55).”
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“Although patients harboring these mutations have a high response rate to the EGFR inhibitors gefitinib and erlotinib, the duration of the response is not long, and patients relapse after about a year of treatment (Pao and Chmielecki 2010).”
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“However, in a previous study >20% of patients demonstrated resistance to EGFR TKIs and all tumors ultimately developed resistance following the initial response (21).”
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“Meta-analysis Background Nonsmall-cell lung cancer (NSCLC), which can be subdivided into squamous cell carcinoma, large cell carcinoma, and adenocarcinoma, is a major histological subtype of lung cancer cells and account for approximately 80 % of all lung cancer cells [1, 2].”
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“For example, it is overexpressed in ~80% of non-small cell lung cancer (NSCLC) [10, 11] and mutated in 20% of NSCLC [12].”
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“However, despite the fact that the majority of patients with EGFR mutations benefited from these drugs, in excess of 20% of patients experienced resistance and all tumors ultimately developed resistance following initial response [10].”
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Resistance to EGFR Inhibitors: Fitness, Competition, and Diversity
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c-Src Increases the Sensitivity to TKIs in the EGFR-Mutant Lung Adenocarcinoma
Min, W., He, C., Zhang, S., & Zhao, Y. (2021) · Frontiers in Oncology · doi:10.3389/fonc.2021.602900 · Cited by 6
“EMT Epithelial-mesenchymal transition Tyr Tyrosine NSCLC Non–small cell lung cancer WT Wild type EGFR Epidermal growth factor receptor PI3K Phosphoinositide-3 kinase AKT Protein kinase B MAPK Mitogen-activated protein kinase ERK1/2 or ERK Extracellular signal-regulated kinase MEK MAPK/ERK kinase FAK Focal adhesion kin…”
BackgroundInfluentialNath, R., Baishya, S., Nath, D., Nahar, L., Sarker, S. D., Choudhury, M. D., & Talukdar, A. D. (2023) · Phytochemical Analysis · doi:10.1002/pca.3254 · Cited by 6
Familial rare EGFR-mutant lung cancer syndrome: Review of literature and description of R776H family
Gabriel, L., McVeigh, T. P., MacMahon, S. W., Avila, Z., Donovan, L., Hunt, I., Draper, A., Minchom, A. R., Popat, S., Davidson, M., et al. (2024) · Lung Cancer · doi:10.1016/j.lungcan.2024.107543 · Cited by 6
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Zhu, W., Pei, J., & Lu, X. (2024) · Expert Opinion on Therapeutic Patents · doi:10.1080/13543776.2024.2446220 · Cited by 6
“Studies have demonstrated that activating mutations in EGFR are detected in more than 20% of NSCLC patients, underscoring the significance of specifically targeting EGFR as a therapeutic strategy [4,5].”
InfluentialChemotherapy and targeted therapy near the end of life affects aggressiveness of palliative care
Zhang, Z., Chen, M., Liu, M.-H., & Cheng, W. (2021) · Annals of Palliative Medicine · doi:10.21037/apm-20-1845 · Cited by 6
“Successful therapies that target patients with anaplastic lymphoma kinase rearrangements or epidermal growth factor receptor mutations have been developed (19-21).”
BackgroundDiscovery and optimization of covalent EGFR T790M/L858R mutant inhibitors
Hoogenboom, N., Demont, D., de Zwart, E., Verkaik, S., Hoek, M. E.-V., van de Kar, B., Kaptein, A., & Barf, T. A. (2021) · Bioorganic & Medicinal Chemistry Letters · doi:10.1016/j.bmcl.2021.128406 · Cited by 6
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Quinton, C. L., & Ellis, P. M. (2011) · Cancers · doi:10.3390/cancers3033506 · Cited by 6
“Initial approaches to the management of lung cancer administered identical combination chemotherapy, regardless of histology, to patients with NSCLC and small-cell lung cancer (SCLC) alike [1,2].”
BackgroundThe Evolving Role of Targeted Therapy in Early-Stage and Locally Advanced Non-small Cell Lung Cancer
West, H. (2011) · Current Oncology Reports · doi:10.1007/s11912-011-0181-0 · Cited by 6
Flow cytometry applications in the study of immunological lung disorders.
Mortaz, E., Gudarzi, H., Tabarsi, P., Adcock, I. M., Masjedi, M. R., Jamaati, H., Garssen, J., Velayati, A. A., & Redegeld, F. A. (2015) · PubMed · Cited by 6
CUSTOM-SEQ: a prototype for oncology rapid learning in a comprehensive EHR environment
Warner, J. L., Wang, L. L., Pao, W. J., Sosman, J. A., Atreya, R. V., Carney, P., & Levy, M. A. (2016) · Journal of the American Medical Informatics Association · doi:10.1093/jamia/ocw008 · Cited by 5
“46 Future work will incorporate this information, especially as findings of in vitro resistance are confirmed in clinical settings or in large collaborative efforts such as ClinGen.”
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A blood biomarker for monitoring response to anti-EGFR therapy
Hughes, N. P., Xu, L., Nielsen, C. H., Chang, E., Hori, S. S., Natarajan, A., Lee, S. C., Kjær, A., Kani, K., Wang, S. X., et al. (2018) · Cancer Biomarkers · doi:10.3233/cbm-171149 · Cited by 6
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Identification of LBX2 as a novel causal gene of lung adenocarcinoma
Hu, J., Bai, Y., Zhang, Q., Li, M., Yin, R. H., & Xu, L. (2020) · Thoracic Cancer · doi:10.1111/1759-7714.13506 · Cited by 6
Messeha, S. S., Nezami, M. A., Hager, S. J., & Soliman, K. F. A. (2021) · Anticancer Research · doi:10.21873/anticanres.15502 · Cited by 6
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“The predominant resistance mechanism for first- and secondgeneration EGFR TKIs is the EGFR T790M mutation.(2) Although osimertinib is active against EGFR-sensitizing therapies after progression on EGFR TKIs without T790M mutation.”
BackgroundA Review on EGFR-Tyrosine Kinase Inhibitors and their Resistance Mechanisms
Naim, M. J., & Samad, A. (2025) · Current Pharmaceutical Design · doi:10.2174/0113816128349342250121053445 · Cited by 5
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Lei, Q., Zhou, X., Li, Y., Zhao, S., Yang, N., Xiao, Z., Song, C., Yu, Q., & Deng, H. (2025) · Journal of the American Chemical Society · doi:10.1021/jacs.4c16528 · Cited by 5
Biswas, R., Yang, C., Lü, W., He, J., Chen, T., Tian, F., & Li, Y. (2021) · European Journal of Integrative Medicine · doi:10.1016/j.eujim.2021.101368 · Cited by 5
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Machine learning method aided discovery of the fourth-generation EGFR inhibitors
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“The molecular structure of ducoarmycins and their derivatives was characterized, including their stereochemistry, through modern analytical techniques [86, 87].”
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“However, among tumors that initially respond to EGFR‑TKIs, the majority of patients eventually acquire resistance, often due to the emergence of a secondary mutation, such as T790M, in the kinase domain of EGFR (8).”
Multiple Myeloma Emerging after Prolonged Gefitinib Treatment for Non-Small Cell Lung Carcinoma
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Molecular Pathology of Non–Small Cell Lung Cancer
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Establishment and characterization of a lung cancer cell line, SMC-L001, from a lung adenocarcinoma
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“Studies on the molecular and cellular biology of lung cancer have demonstrated that some tumors can be highly dependent or addicted to specific oncogenes for growth and survival, despite the diverse array of genetic lesions that occur (Pao and Chmielecki 2010).”
BackgroundAntibody-Mediated Receptor Endocytosis: Harnessing the Cellular Machinery to Combat Cancer
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“Lung cancer is a leading cause of cancerrelated death worldwide [1, 2].”
Background
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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