EGFR L718Q mutation occurs without T790M mutation in a lung adenocarcinoma patient with acquired resistance to osimertinib

Abstract

Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) improve the clinical outcomes of EGFR-mutant non-small cell lung cancer (NSCLC) patients significantly, however, acquired resistance occurs almost inevitably. The underlying mechanisms of osimertinib resistance and treatment strategies after resistance remain largely unknown. Here we reported a case of lung adenocarcinoma patient who progressed on osimertinib with EGFR L718Q mutation in the absence of T790M mutation. The patient received icotinib as an exploratory treatment regimen for a short while with stable disease observed. Unfortunately, the therapy was discontinued due to intolerable hepatotoxicity. This is the first clinical report of the use of the effective EGFR-TKI treatment after L718Q-induced osimertinib resistance. The therapeutic regimens for NSCLC patients progressed on osimertinib still require large-scale investigation.

Keywords: EGFR L718Q; Non-small cell lung cancer (NSCLC); epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs); osimertinib resistance.

Figure 1

The integrated genome viewer revealed the mutational status of tumor after osimertinib therapy. (A) EGFR L858R mutation; (B) wild-type EGFR T790; (C) EGFR L718Q mutation.

Figure 2

CT scan images demonstrated an increase in size of lesions on the inferior lobe of left lung and stabilization of nodules in right lung after 1-month treatment of icotinib. (A) Before treatment initiation; (B) after treatment.