Cited by 687HER2/EGFR in Cancer ResearchLung Cancer Treatments and MutationsColorectal Cancer Treatments and Studies

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Understanding resistance to EGFR inhibitors—impact on future treatment strategies

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Wheeler, Deric L., Dunn, Emily F., Harari, Paul M.·2010·Nature Reviews Clinical Oncology

DOI 10.1038/nrclinonc.2010.97PMC PMC2929287

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Abstract

EGFR is a tyrosine kinase that participates in the regulation of cellular homeostasis. Following ligand binding, EGFR stimulates downstream cell signaling cascades that influence cell proliferation, apoptosis, migration, survival and complex processes, including angiogenesis and tumorigenesis. EGFR has been strongly implicated in the biology of human epithelial malignancies, with therapeutic applications in cancers of the colon, head and neck, lung, and pancreas. Accordingly, targeting EGFR has been intensely pursued, with the development of a series of promising molecular inhibitors for use in clinical oncology. As is common in cancer therapy, challenges with respect to treatment resistance emerge over time. This situation is certainly true of EGFR inhibitor therapies, where intrinsic and acquired resistance is now well recognized. In this Review, we provide a brief overview regarding the biology of EGFR, preclinical and clinical development of EGFR inhibitors, and molecular mechanisms that underlie the development of treatment resistance. A greater understanding of the mechanisms that lead to EGFR resistance may provide valuable insights to help design new strategies that will enhance the impact of this promising class of inhibitors for the treatment of cancer.

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Additional file 6 of Lattice complex assembled by noncompetitive anti-EGFR antibodies regulates actin cytoskeletal reorganization
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Additional file 5 of Lattice complex assembled by noncompetitive anti-EGFR antibodies regulates actin cytoskeletal reorganization
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Additional file 8 of Lattice complex assembled by noncompetitive anti-EGFR antibodies regulates actin cytoskeletal reorganization
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Additional file 1 of AXL regulates neuregulin1 expression leading to cetuximab resistance in head and neck cancer
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Additional file 1 of Lattice complex assembled by noncompetitive anti-EGFR antibodies regulates actin cytoskeletal reorganization
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Additional file 2 of CircHIF1A induces cetuximab resistance in colorectal cancer by promoting HIF1α-mediated glycometabolism alteration
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Additional file 4 of CircHIF1A induces cetuximab resistance in colorectal cancer by promoting HIF1α-mediated glycometabolism alteration
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Additional file 2 of AXL regulates neuregulin1 expression leading to cetuximab resistance in head and neck cancer
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Additional file 7 of Lattice complex assembled by noncompetitive anti-EGFR antibodies regulates actin cytoskeletal reorganization
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BindingDB Entry 50047412: Computer-aided design, synthesis, and biological evaluation of new indole-2-carboxamide derivatives as PI3Ka/EGFR inhibitors.
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BindingDB Entry 50048120: Synthesis and investigation of novel 6-(1,2,3-triazol-4-yl)-4-aminoquinazolin derivatives possessing hydroxamic acid moiety for cancer therapy.
BindingDB (2018) · UC San Diego · doi:10.7270/q22n548x
Enhancing radiosensitivity in head and neck cancer by inhibition of growth factor receptor signaling EGFR and beyond
Stegeman, H. (2013) · Radboud Repository (Radboud University)
WITHAFERIN A: A NOVEL THERAPEUTIC APPROACH FOR MALIGANT BRAIN TUMORS
Grogan, P. T. (2014) · KU ScholarWorks (The University of Kansas)
Molecular Testing in Pulmonary Tumors
Tanguay, J., Karimi, S., Hwang, D. M., & Tsao, M. (2014) · Springer eBooks · doi:10.1007/978-1-4899-8050-2_13

Authors: Wheeler, D. L., Dunn, E. F., & Harari, P. M.
Affiliations: University of Wisconsin–Madison (US)
Corresponding author: Wheeler, Deric L.
ORCID: Wheeler, Deric L.
Dunn, Emily F.
Harari, Paul M.
Venue: Nature Reviews Clinical Oncology
Publisher: Springer Science and Business Media LLC
Published: 2010-06-15
Volume: 7
Issue: 9
Pages: 493-507
ISSN: 1759-4774 (ISSN-L)
1759-4782
DOI: 10.1038/nrclinonc.2010.97
PMC: PMC2929287
OpenAlex: W2053439872
Cited by: 683
References: 182
Citations by year: 2026: 21 · 2025: 20 · 2024: 35 · 2023: 29 · 2022: 31 · 2021: 29 · 2020: 44 · 2019: 25 · 2018: 36 · 2017: 50 · 2016: 46 · 2015: 61 · 2014: 66 · 2013: 68 · 2012: 64
FWCI: 6.61
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature Reviews Clinical Oncology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (5t32ca009614-25)
U.S. Public Health Service (P30CAO14520)
National Cancer Institute (T-32 CA 0096-14, R01CA113448)
National Center for Research Resources (UL1RR025011)
Topics: Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
Keywords: EGFR inhibitors, EGFR, acquired drug resistance, intrinsic resistance, tyrosine kinase inhibitors, resistance mechanisms, EGFR signaling, epithelial malignancies, lung cancer, head and neck cancer, colon cancer, pancreatic cancer, combination therapy
MeSH terms: Cetuximab, Erlotinib Hydrochloride, Gefitinib, Panitumumab, Antibodies, Monoclonal, Antineoplastic Agents, Humans, Neoplasms, Proto-Oncogene Proteins, Quinazolines, Proto-Oncogene Proteins p21(ras), Treatment Outcome, Disease Progression, ras Proteins, Drug Resistance, Neoplasm, Protein Kinase Inhibitors, Antibodies, Monoclonal, Humanized, ErbB Receptors

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