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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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“Epidermal growth factor receptor (EGFR) mutations are the most commonly identified mutation in NSCLC, occurring in 10–15% of all NSCLC cases [3].”
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“NSCLC includes adenocarcinoma, squamous cell carcinoma and large‐cell carcinoma (Pao and Chmielecki, 2010).”
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“These 209 may be used as monotherapies or as combination therapy (47-49).”
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“…outgrowth of tumor cells with mutations in the drug target represents a well documented mechanism of acquired kinase inhibitor resistance in other cancer types, for example EGFR mutant lung cancer (Pao and Chmielecki, 2010), direct evidence for such acquired resistance is currently lacking in GBM.”
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“More than 60% of NSCLC patients are diagnosed to have advanced or metastatic tumors, which are unsuitable for surgical resection with curative intent (Tong, 2006; Pao and Chmielecki, 2010).”
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“A favorable clinical benefit occurs more frequently in EGFR-mutated lung adenocarcinoma than in EGFR-wild-type lung adenocarcinoma patients (13).”
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“Epidermal growth factor receptor (EGFR) is often overexpressed or mutated in a variety of cancers, like lung cancer and colorectal cancer [13, 14], and this leads to enhanced activation and tumorigenesis.”
BackgroundmTOR Inhibitors Control the Growth of EGFR Mutant Lung Cancer Even after Acquiring Resistance by HGF
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“In addition, 20–30% of the patients show unfavorable responses, although their tumors have target mutations (intrinsic resistance) [5].”
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“Several generations of TKIs have been developed and these drugs are superior to conventional chemotherapy in prolonging progression-free survival (PFS) of NSCLC patients harboring common EGFR mutations, including exon 19 deletions (Del19) and L858R [3].”
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“EGFR mutations were the first molecular alterations in NSCLC, discovered in 2004 [7], and they occur in 10–28% of NSCLC patients [8].”
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“74 (sensitive [22, 23]) −17 % Second scan E+ Yes Yes NA Synthesis of [(15)O]H2O failed quality check 13”
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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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