The DOI matches its Crossref record; 181 of the 181 references it cites were found in a registry or an index.
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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Cites
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“Approximately 2–3% of NSCLCs harbour mutations in BRAF , which encodes a signalling molecule downstream of EGF”
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Paclitaxel–Carboplatin Alone or with Bevacizumab for Non–Small-Cell Lung Cancer
Sandler, A., Gray, R., Perry, M. C., Brahmer, J., Schiller, J. H., Dowlati, A., Lilenbaum, R., & Johnson, D. H. (2006) · New England Journal of Medicine · doi:10.1056/nejmoa061884 · Cited by 5,761
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“Another 5% of tumours harbour translocations in anaplastic lymphoma kinase ( ALK”
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Flagged first, then by citations
Research works printed but not linked: 1
- Oh, I.-J. et al. in AACR–IASLC Joint Conference on Molecular Origins of Lung Cancer: Prospects for Personalized Prevention and Therapy (Coronado, California USA, 2010).
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Rosell, R., Carcereny, E., Gervais, R., Vergnenegre, A., Massuti, B., Felip, E., Palmero, R., Garcia-Gomez, R., Pallares, C., Sanchez, J. M., et al. (2012) · The Lancet Oncology · doi:10.1016/s1470-2045(11)70393-x · Cited by 5,489
The causes and consequences of genetic heterogeneity in cancer evolution
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“Mutations in EGFR occur in 10% to 35% of NSCLCs and confer sensitivity to the EGFR TKIs erlotinib, gefitinib, and afatinib (6).”
InfluentialSelf-citationMapping the Hallmarks of Lung Adenocarcinoma with Massively Parallel Sequencing
Imielinski, M., Berger, A. H., Hammerman, P. S., Hernandez, B., Pugh, T. J., Hodis, E., Cho, J., Suh, J., Capelletti, M., Sivachenko, A., et al. (2012) · Cell · doi:10.1016/j.cell.2012.08.029 · Cited by 1,789
“…routinely used to guide clinical care of lung adenocarcinoma patients, largely due to clinical trials that demonstrated superior efficacy of targeted kinase inhibitors as compared to standard chemotherapy for patients with EGFR mutations or ALK fusions (Kwak et al., 2010; Pao and Chmielecki, 2010).”
BackgroundSelf-citationIntegrative genome analyses identify key somatic driver mutations of small-cell lung cancer
Peifer, M., Fernandez‐Cuesta, L., Sos, M. L., George, J., Seidel, D., Kasper, L. H., Plenker, D., Leenders, F., Sun, R., Zander, T., et al. (2012) · Nature Genetics · doi:10.1038/ng.2396 · Cited by 1,404
Self-citation
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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