Acquired EGFR C797S mutation mediates resistance to AZD9291 in non–small cell lung cancer harboring EGFR T790M
Open accessAbstract
Here we studied cell-free plasma DNA (cfDNA) collected from subjects with advanced lung cancer whose tumors had developed resistance to the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) AZD9291. We first performed next-generation sequencing of cfDNA from seven subjects and detected an acquired EGFR C797S mutation in one; expression of this mutant EGFR construct in a cell line rendered it resistant to AZD9291. We then performed droplet digital PCR on serial cfDNA specimens collected from 15 AZD9291-treated subjects. All were positive for the T790M mutation before treatment, but upon developing AZD9291 resistance three molecular subtypes emerged: six cases acquired the C797S mutation, five cases maintained the T790M mutation but did not acquire the C797S mutation and four cases lost the T790M mutation despite the presence of the underlying EGFR activating mutation. Our findings provide insight into the diversity of mechanisms through which tumors acquire resistance to AZD9291 and highlight the need for therapies that are able to overcome resistance mediated by the EGFR C797S mutation.
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Identification of the C797S mutation in patients with lung cancer, whose tumours had developed resistance to AZD9291, was identified by Thress et al using NGS in cfDNA samples.
“Identification of the C797S mutation in patients with lung cancer, whose tumours had developed resistance to AZD9291, was identified by Thress et al57 using NGS in cfDNA samples.”
From Mechanisms of resistance to EGFR-targeted drugs: lung cancer (2016) · cites this paper as [57]
C797S mutations have been shown to cause resistance to mutant-selective EGFR inhibitors (WZ4002, rociletinib, osimertinib) in vitro and in lung cancer patients.
“Mutations in C797 (to C797S) have recently been demonstrated to lead to resistance to mutant selective EGFR inhibitors both in vitro (WZ4002, rociletinib, osimertinib) and in lung cancer patients (31, 33).”
From Response Heterogeneity of EGFR and HER2 Exon 20 Insertions to Covalent EGFR and HER2 Inhibitors (2017) · cites this paper as [33]
Mutations in this conserved cysteine residue may be a common mechanism of acquired resistance to covalent kinase inhibitors.
“suggesting that mutations in this conserved residue may be a common mechanism of acquired resistance to covalent kinase inhibitors (37).”
From EGFR Mutations and Resistance to Irreversible Pyrimidine-Based EGFR Inhibitors (2015) · cites this paper as [37]
C481S mutations have been identified in chronic lymphocytic leukemia patients treated with ibrutinib.
“recent studies have also identified mutations in C481 (C481S), the analogous cysteine residue to C797 in EGFR, in patients with chronic lymphocytic leukemia treated with the Bruton’s tyrosine kinase (BTK) inhibitor ibrutinib”
From EGFR Mutations and Resistance to Irreversible Pyrimidine-Based EGFR Inhibitors (2015) · cites this paper as [37]
C797S secondary mutation was detected in T790M-positive tumors that acquired resistance to osimertinib.
“C797S secondary mutation was detected in T790M‐positive tumors that acquired resistance to osimertinib.40”
From Not all epidermal growth factor receptor mutations in lung cancer are created equal: Perspectives for individualized treatment strategy (2016) · cites this paper as [40]
Sanger sequencing can detect known and novel EGFR mutations, such as C797S, in the setting of resistance to third-generation EGFR TKIs.
“whereas Sanger sequencing may uncover known and novel mutations (e.g., C797S) in the context of resistance to third-generation EGFR TKIs.39”
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- Authors
- Thress, K. S., Paweletz, C. P., Felip, E., Cho, B. C., Stetson, D., Dougherty, B., Lai, Z., Markovets, A., Vivancos, A., Kuang, Y., Ercan, D., Matthews, S. E., Cantarini, M., Barrett, J. C., Jänne, P. A., & Oxnard, G. R.
- Affiliations
- AstraZeneca (United States) (US)
- Dana-Farber Cancer Institute (US)
- Vall d'Hebron Hospital Universitari (ES)
- Yonsei University (KR)
- Vall d'Hebron Institute of Oncology (ES)
- AstraZeneca (United Kingdom) (GB)
- Corresponding author
- Oxnard, Geoffrey R
- ORCID
- Venue
- Nature Medicine
- Published
- 2015-05-04
- Volume
- 21
- Issue
- 6
- Pages
- 560-562
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC4771182
- OpenAlex
- W1546552389
- Cited by
- 1,589
- References
- 16
- Citations by year
- 2026: 99 · 2025: 111 · 2024: 96 · 2023: 92 · 2022: 134 · 2021: 159 · 2020: 178 · 2019: 167 · 2018: 182 · 2017: 178 · 2016: 148 · 2015: 44
- FWCI
- 146.26
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- YUHSpace (Yonsei University Medical Library) (submittedVersion, cc-by-nc-nd)
- Funders
- AstraZeneca
- National Cancer Institute (P01CA129243, R01CA114465, R01CA135257, P01CA154303)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Keywords
- C797S mutation, acquired resistance, osimertinib, T790M mutation, non-small cell lung cancer, EGFR tyrosine kinase inhibitors, plasma cell-free DNA, liquid biopsy, droplet digital PCR, EGFR activating mutations
- MeSH terms
- Acrylamides, Adult, Aged, Aniline Compounds, Carcinoma, Non-Small-Cell Lung, Female, Humans, Indoles, Male, Middle Aged, Mutation, Pyrimidines, Drug Resistance, Neoplasm, High-Throughput Nucleotide Sequencing, ErbB Receptors
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