Abstract
Epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) is one of the most important targeted drugs for lung cancer patients carrying EGFR sensitive mutations. However, almost all patients that are effective to this treatment will eventually develop secondary resistance to EGFR-TKI. The most accepted mechanisms of resistance mainly include T790M mutation, MET amplification, PIK3CA mutation, down-regulation of PTEN expression and activation of Fas-transcription factor-κB. Recent years, many new drugs are developed to overcome this resistance. Although most of drugs are in the stages of cell or animal experiment, some new drugs get positive clinical results. Key words: Lung neoplasms; Drug resistance, neoplasm; EGFR-TKI
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