NSCLC harboring EGFR exon‐20 insertions after the regulatory C‐helix of kinase domain responds poorly to known EGFR inhibitors
Abstract
Anecdote clinical observations hint that non‐small cell lung cancer (NSCLC) with exon‐20 insertions might respond poorly to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), contrasting to those with classic mutations. Lack of patient‐derived experimental models has been a major hurdle for the discovery of new treatment for the diseases. We established two NSCLC‐PDXs harboring two different exon‐20 insertions, LU0387‐adenocarcinoma (ADC) with a nine‐base insertion at 2319 (H773‐V774insNPH) and LU3075‐squamous cell carcinoma (SCC) with a nine‐base insertion at 2316 (P772‐H773insDNP). Both insertions immediately follow the regulatory C‐helix of the kinase domain. Contrary to the generally good responses to EGFR inhibitors observed in PDXs with classic mutations, both exon‐20 insertions are largely resistant to cetuximab and TKIs in vivo, suggesting fundamental difference from the classic EGFR mutations, consistent with the poor response rate to TKI seen in anecdotal clinic reports. It is worth noting that although responses are generally poor, they differ between the two exon‐20 mutants depending on the type of TKI. In vitro drug sensitivity assays using established primary cell lines from our two PDXs largely confirmed the in vivo data. Our data from patient‐derived experimental models confirmed that exon‐20 insertions in domain immediately following the C‐helix confer poor response to all known EGFR inhibitors, and suggested that these models can be utilized to facilitate the discovery of new therapies targeting NSCLC harboring exon‐20 insertions.
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In a PDX model of NSCLC driven by an EGFR exon 20 mutation with insertions in the loop after the α-C helix (EGFR H773insNPH), third-generation EGFR TKIs osimertinib and rociletinib had minimal activity.
“Moreover, in a patient-derived xenograft (PDX) model of NSCLC driven by an EGFR exon 20 mutation in which the insertions are in the loop after the α-C helix (EGFR H773insNPH), the third-generation EGFR TKIs osimertinib (AZD9291) and rociletinib (CO-1696) were found to have minimal activity28.”
From Mechanisms and clinical activity of an EGFR and HER2 exon 20–selective kinase inhibitor in non–small cell lung cancer (2018) · cites this paper as [28]
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- Authors
- Yang, M., Xu, X., Cai, J., Ning, J., Wery, J. P., & Li, Q.
- Affiliations
- Crown Bioscience, Inc 3375 Scott Blvd, Suite 108, Santa Clara CA
- Peking University (CN)
- Corresponding author
- Li, Qi‐Xiang
- Venue
- International Journal of Cancer
- Publisher
- Wiley
- Published
- 2016-03-25
- Volume
- 139
- Issue
- 1
- Pages
- 171-176
- ISSN
- 0020-7136 (ISSN-L)
- 1097-0215
- OpenAlex
- W2274623524
- Cited by
- 55
- References
- 24
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 6 · 2023: 3 · 2022: 6 · 2021: 6 · 2020: 7 · 2019: 9 · 2018: 7 · 2017: 1 · 2016: 4
- FWCI
- 6.26
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- International Journal of Cancer (publishedVersion)
- PubMed (publishedVersion)
- 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 exon 20 insertion, non-small cell lung cancer, EGFR tyrosine kinase inhibitors, cetuximab resistance, patient-derived xenografts, drug resistance, EGFR mutation, squamous cell carcinoma, adenocarcinoma, drug sensitivity
- MeSH terms
- Adenocarcinoma, Carcinoma, Non-Small-Cell Lung, Carcinoma, Squamous Cell, Exons, Humans, Mutation, Quinazolines, Drug Resistance, Neoplasm, Xenograft Model Antitumor Assays, Cell Line, Tumor, Protein Kinase Inhibitors, ErbB Receptors
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