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Onco Targets Ther. 2018 Dec 18;12:51-56. doi: 10.2147/OTT.S188612. eCollection 2019.

Newly emergent acquired EGFR exon 18 G724S mutation after resistance of a T790M specific EGFR inhibitor osimertinib in non-small-cell lung cancer: a case report.

Author information

Department of Respiratory Medicine, Xiangya Hospital (Key Cite of National Clinical Research Center for Respiratory Disease), Central South University, Changsha, Hunan, P.R. China,;
Department of Gerontology, Xiangya Hospital, Central South University, Changsha, Hunan, P.R. China.



T790M mutation is well known as the most common mechanism for resistance to the first- and second-generation tyrosine kinase inhibitors (TKIs) for EGFR mutation in non-small-cell lung cancer. Several third-generation EGFR TKIs, such as osimertinib, have been explored and approved for conquering this resistance; however, acquired resistance to osimertinib is evident and the resistance mechanisms remain complex and incompletely explored.

Case presentation:

A non-smoking 58-year-old female patient was initially diagnosed with lung adenocarcinoma harboring EGFR exon 19 deletion and clinically responded to initial gefitinib treatment. The patient progressed on gefitinib after >1 year and a T790M mutation was detected in tissue biopsy by next-generation sequencing (NGS). Osimertinib treatment was administrated for several months and an acquired rare EGFR G724S mutation was detected via NGS blood sample after osimertinib resistance.


The specific mechanisms of acquiring drug resistance for EGFR-TKIs have not been fully explored. EGFR G724S mutation might be associated with osimertinib resistance but more studies about the mechanism should be explored.


EGFR mutation; NSCLC; next-generation sequencing; tyrosine kinase inhibitor

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