Analysis of acquired resistance mechanisms to osimertinib in patients with EGFR-mutated advanced non-small cell lung cancer from the AURA3 trial

Juliann Chmielecki, Tony Mok, Yi-Long Wu, Ji-Youn Han, Myung-Ju Ahn, Suresh S. Ramalingam, Thomas John, Isamu Okamoto, James Chih-Hsin Yang, Frances A. Shepherd, Krishna C. Bulusu, Gianluca Laus, Barbara Collins, J. Carl Barrett, Ryan J. Hartmaier and Vassiliki Papadimitrakopoulou ()
Additional contact information
Juliann Chmielecki: Translational Medicine, Oncology R&D, AstraZeneca
Tony Mok: Chinese University of Hong Kong
Yi-Long Wu: Guangdong Provincial People’s Hospital & Guangdong Academy of Medical Sciences
Ji-Youn Han: National Cancer Center
Myung-Ju Ahn: Sungkyunkwan University School of Medicine
Suresh S. Ramalingam: Emory University School of Medicine
Thomas John: Medical Oncology, Olivia Newton-John Cancer Research Institute, Austin Health
Isamu Okamoto: Kyushu University
James Chih-Hsin Yang: National Taiwan University Cancer Center
Frances A. Shepherd: Princess Margaret Cancer Centre, and the University of Toronto
Krishna C. Bulusu: Translational Medicine, Oncology R&D, AstraZeneca
Gianluca Laus: Translational Medicine, Oncology R&D, AstraZeneca
Barbara Collins: Biometrics and Information Sciences, AstraZeneca
J. Carl Barrett: Translational Medicine, Oncology R&D, AstraZeneca
Ryan J. Hartmaier: Translational Medicine, Oncology R&D, AstraZeneca
Vassiliki Papadimitrakopoulou: University of Texas M.D. Anderson Cancer Center

Nature Communications, 2023, vol. 14, issue 1, 1-8

Abstract: Abstract Osimertinib, an epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI), potently and selectively inhibits EGFR-TKI-sensitizing and EGFR T790M resistance mutations. This analysis evaluates acquired resistance mechanisms to second-line osimertinib (n = 78) in patients with EGFR T790M advanced non-small cell lung cancer (NSCLC) from AURA3 (NCT02151981), a randomized phase 3 study comparing osimertinib with chemotherapy. Plasma samples collected at baseline and disease progression/treatment discontinuation are analyzed using next-generation sequencing. Half (50%) of patients have undetectable plasma EGFR T790M at disease progression and/or treatment discontinuation. Fifteen patients (19%) have >1 resistance-related genomic alteration; MET amplification (14/78, 18%) and EGFR C797X mutation (14/78, 18%).

Date: 2023
References: View complete reference list from CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-023-35962-x Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-35962-x

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-023-35962-x

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().