Abstract
In the era of personalized medicine, epidermal growth factor receptor (EGFR) inhibition with tyrosine kinase inhibitor (TKI) has been a mainstay of treatment for non-small cell lung cancer (NSCLC) patients with an EGFR mutation. Acquired resistance, especially substitution of methionine for threonine at position 790 (T790M), which has accounted for more than half of the cases, developed inevitably in patients who were previously treated with EGFR-TKI. At present, there is no standard treatment for patients who have developed a resistance to EGFR-TKI. Several strategies have been developed or suggested to treat such patients. This article aimsto review the EGFR-TKI re-treatment strategy and the efficacy of different generations of EGFR-TKIs in patients with acquired resistance to prior EGFR-TKI.
Highlights
Lung cancer is the leading cause of global cancer death
The findings of the high efficacy of epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) treatment in patients with activating EGFR mutations have had a great influence on the paradigm of non-small cell lung cancer (NSCLC) treatment
The subgroup analysis was more in favor of dacomitinib in the EGFR mutation group (hazard ration (HR) = 0.46; 95% CI, 0.18 to 1.18)
Summary
Lung cancer is the leading cause of global cancer death. Patients are diagnosed mostly with non-small cell lung cancer (NSCLC) and usually have a poor prognosis [1,2]. The discovery of a mutation on the epidermal growth factor receptor (EGFR) gene made a huge difference in the treatment strategy for NSCLC, especially adenocarcinoma. About 10% to 15% of patients harboring an activating EGFR mutation are from Western societies [9], and about 50% are Asian [10,11]. The findings of the high efficacy of EGFR-TKI treatment in patients with activating EGFR mutations have had a great influence on the paradigm of NSCLC treatment. There is currently no standard treatment for patients resistant to EGFR-TKI. We want to review re-treatment with EGFR-TKI in NSCLC patients with activating EGFR mutation
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