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Abstract
Epidermal growth factor receptor (EGFR) mutations in patients with non-small cell lung cancer (NSCLC) usually develop disease progression after a median of 10 to 14 mo on tyrosine kinase inhibitor (TKI). Several mechanisms of resistance to TKI have been described, threonine-methionine substitution at position 790 (T790M), mesenchymal–epithelial transition factor (MET) amplification, overexpression of hepatocyte growth factor (HGF), upregulation of insulin-like growth factor (IGF) receptor signaling, transformation to small cell lung cancer, and so on. A variety of different therapeutic approaches aimed at overcoming resistance are motivated, irreversible EGFR inhibitors, combination with EGFR targeted antibodies, mesenchymal–epithelial transition factor (MET) inhibitors, HGF inhibitors, and so forth. Nevertheless, the results were not optimistic. Here we report a case of reversion of erlotinib-acquired resistance twice, and had a good improvement of outcomes every time. There are some possible reasons for this phenomenon. Considering this report, the patients who acquired resistance after retreatment of EGFR-TKI, using EGFR-TKI repeatedly may be a choice selectively.
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Disclosure of Potential Conflicts of Interest
No potential conflicts of interest were disclosed.
Acknowledgments
This work was supported by The National Natural Science Foundation, 81201827.