In 2004, several groups reported the correlation between EGFR mutations and sensitivity to EGFR tyrosine kinase inhibitors (EGFR-TKIs). Since then, multiple EGFR-TKIs have been developed, improving the prognosis of advanced EGFR-mutated lung cancer patients. However, most patients with advanced EGFR mutation-positive lung cancer die of lung cancer in less than five years, highlighting the need for the further development of effective therapies. To develop effective inhibitors or treatment strategies, a basic understanding of EGFR-mutated lung cancer is essential. In particular, the knowledge of how EGFR mutations activate EGFR kinase and how sensitivity to EGFR-TKIs is determined is important. In this review, I will summarize the knowledge and propose clinical insight on how to translate this basic knowledge into a clinical setting.
- Activation mechanism
- Drug sensitivity
- Enzyme activity
- Epidermal growth factor receptor
ASJC Scopus subject areas